Pharm Module 3

Variant angina -- patho and treatment strategy

(Prinzmetal's angina or vasospastic angina) PATHO Caused by coronary artery spasm, which restricts blood flow to the myocardium Pain is secondary to insufficient oxygenation of the heart Can produce pain at any time Frequently, variant angina occurs in conjunction with stable angina TREATMENT STRATEGY Goal: reduce incidence and severity of attacks Treated by increasing the cardiac oxygen supply with vasodilators, which prevent or relieve coronary artery spasm

Bile acid sequestrants (mechanism of action, clinical indications, side effects)

(colesevelam) Mechanism of action: increase LDL receptors on hepatocytes, prevents reabsorption of bile acids Clinical indications: adjunct therapy to diet and exercise for reducing LDL cholesterol in patients with primary hypercholesterolemia; primarily used as an adjunct to statins Side effects: constipation, bloating

Fibric acid derivatives (mechanism of action, clinical indications, side effects)

(gemfibrozil, fenofibrate, fenofibric acid) Most effective drugs for lowering TG levels Can raise HDL cholesterol, little/no effect on LDL Mechanism of action: appear to block receptors Clinical indications: reduction of high levels of plasma triglycerides (VLDLs), raise HDL Side effects: can increase risk for bleeding in patients taking warfarin, can increase risk for rhabdo in patients taking statins, rash, GI disturbances, gallstones, myopathy, liver injury

Adrenergic receptors

(part of the peripheral → autonomic → sympathetic nervous system) = alpha1, alpha2, beta1, and beta2

Mechanism of action of reserpine

*Adrenergic neuron-blocking agent* Mechanism of action: causes depletion of norepi from postganglionic sympathetic neurons Therefore decreases activation of practically all adrenergic receptors, causing effects closely resembling those produced by a combination of alpha- and beta-adrenergic blockade It depletes NE by 1) acting on vesicles within the nerve terminal to cause displacement of stored NE, thereby exposing the transmitter to destruction by monoamine oxidase, and 2) by blocking the uptake of dopamine, the immediate precursor to NE

Explain adjunctive drug therapy post MI, including the use of anticoagulants.

? MI predisposes heart and vascular system to serious complications: ventricular dysrhythmias, cardiogenic shock, heart failure, cardiac rupture These can be treated with a combination of drugs

Things to consider (adverse effects, contraindications, etc.) with furosemide (Lasix)

ADVERSE EFFECTS -Hyponatremia, hypochloremia, dehydration -Hypotension -Relaxation of venous smooth muscle -Hypokalemia -Ototoxicity CONTRAINDICATIONS/PRECAUTIONS Can cause hyperglycemia -- use with caution in DM Has caused maternal death, fetal death, etc. in animals -- use only if absolutely required in pregnant patients Can cause hyperuricemia -- can cause gouty attack in patients predisposed to gout Lots of drug interactions: digoxin, ototoxic drugs (especially aminoglycoside abx like gent), potassium-sparing diuretics, lithium, NSAIDs

Therapeutic uses for beta blockade

ANGINA PECTORIS (beta blockers are mainstay of antianginal therapy; blocking the receptors decreases cardiac workload, reduces O2 demand, prevent ischemia and pain) HTN Cardiac dysrhythmias MI (Treatment with a beta blocker can reduce pain, infarct size, mortality, and the risk of reinfarction) HEART FAILURE (standard therapy for HF) Hyperthyroidism Migraine prophylaxis Stage fright Pheochromocytoma Glaucoma

Adjunct medications to reperfusion therapy

ANTICOAGULANT -Heparin -Fondaparinux (selective factor Xa inhibitor) as an alternative to heparin -Bivalirudin (direct thrombin inhibitor) is the preferred agent over heparin in patients undergoing PCI who are at high risk for bleeding ANTIPLATELET DRUGS -Thienopridines (clopidogrel, ticagrelor, prasugrel) -Glycoprotein IIb/IIIa inhibitors -Aspirin ACE INHIBITORS and ARBs

Therapeutic uses

ASTHMA Activation of beta2 receptors in the lungs promotes bronchodilation Helps relieve and prevent asthma attacks Some agents (like albuterol) are selective for beta2, and some are less selective (isoproterenol) DELAY OF PRETERM LABOR Activation of beta2 receptors in the uterus relaxes uterine smooth muscle HYPERGLYCEMIA Activation of beta2 receptors in the liver and skeletal muscles leads to breakdown of glycogen into glucose Beta2 agonists cause hyperglycemia only in patients with diabetes

Disturbances of conduction r/t arrhythmias

AV block (first, second and third degree) Reentry

Adverse effects and drug interactions with thiazides

Adverse effects Hyponatremia, hypochloremia, and dehydration Hypokalemia Use in pregnancy and lactation Hyperglycemia Hyperuricemia Impact on lipids, calcium and mag Drug interactions Digoxin Augments effects of hypertensive meds Can reduce renal excretion of lithium (leading to accumulation) NSAIDS may blunt diuretic effect

Describe how excessive vasodilation can cause adverse effects that can actually worsen many of the conditions for which vasodilators are given.

Adverse effects related to vasodilation: postural hypotension, reflex tachycardia, expansion of blood volume Drugs that dilate veins can cause orthostatic hypotension Drugs that dilate arterioles or veins can cause reflex tachycardia, which increases cardiac work and elevates blood pressure (this can be blunted with a beta blocker) Drugs that dilate arterioles or veins can cause fluid retention, which can be blunted with a diuretic

Define and understand what the prodysrhythmic effects of Antidysrhythmic Drugs are.

All antidysrhythmic drugs can worsen existing dysrhythmias and generate new ones Antidysrhythmic drugs should only be used when dysrhythmias are symptomatically significant and only when the potential benefits clearly outweigh the risks Prolonged QT interval is one mechanism that warrants special attention Drugs that prolong QT interval increase risk of torsade de pointes, which can progress to fatal v fib All class IA and class III agents cause QT prolongation, and so must be used with special caution

Therapeutic uses of verapamil

Angina pectoris Essential hypertension Cardiac dysrhythmias

Clinical uses for nifedipine

Angina pectoris HTN Investigational: migraine relief and treatment of preterm labor

Clinical uses for diltiazem

Angina pectoris Hypertension Cardiac dysrhythmias (a-flutter, a-fib, paroxysmal tachycardia)

Adverse effects of beta1 activation

Angina pectoris (because beta1 agonists increase cardiac oxygen demand by increasing the HR and force of contraction, patients with compromised coronary circulation are at risk for angina attack)

Contraindications of ARBs

Angioedema (discontinue and never use again if angioedema occurs) Fetal harm (contraindicated in 2nd and 3rd trimester) Renal failure

The four American College of Cardiology/American Heart Association stages

Based on the observation that HF is a progressive disease that moves through stages of increasing severity Stage A -At high risk for HF but without structural heart disease or symptoms of HF Stage B -Structural heart disease but without symptoms of HF Stage C -Structural heart disease with prior or current symptoms of HF Stage D -Advanced structural heart disease with marked symptoms of HR at rest, and requiring specialized interventions (e.g., heart transplant, mechanical assist device)

Discuss the major adverse effect of aldosterone antagonists.

Because of risk of hyperkalemia, combined use with potassium supplements, salt substitutes, or potassium-sparing diuretics is contraindicated Combo with ACE inhibitors or ARBs should be done with caution Not for use in patients with high serum potassium, or for patients with impaired renal function or type 2 DM with microalbuminuria, both of which can promote hyperkalemia

Ranolazine

Belongs to first new class of antianginal agents approved in more than 25 years Not first-line therapy- combine with other agents when response to first-line agents is inadequate Benefits are modest and greater in men than in women Exact mechanism is unknown Does not reduce HR, BP, or vascular resistance Adverse effects -Can prolong QT interval (multiple drug interactions) -Elevation of BP in patients with severe renal impairment -Constipation, nausea -Dizziness, headache -Drug interactions with CYP3A4 drugs, QT drugs, and CCBs

Vaughan Williams Class II

Beta blockers Reduce calcium entry and depress phase 4 depolarization 3 prominent effects on the heart: In SA node, they reduce automaticity In the AV inode, the slow conduction velocity In the atria and ventricles, they reduce contractility Propranolol, acebutolol, esmolol

How do the following drug types lower BP: beta blockers, CCBs, ACE inhibitors/ARBs/DRIs, aldosterone agonists?

Beta blockers appear to lower BP by reducing peripheral vascular resistance Calcium channel blockers reduce BP by promoting dilation of arterioles ACE inhibitors, ARBs, and DRIs lower BP by preventing angiotensin II-mediated vasoconstriction and aldosterone-mediated volume expansion Aldosterone agonists lower BP by preventing aldosterone-mediated retention of sodium and water in the kidney

Considerations re: other drugs being administered with CCBs

Beta blockers decrease the adverse cardiac effects on nifedipine but can intensify the adverse cardiac effects of verapamil and diltiazem Use verapamil and diltiazem with caution in patients with heart failure or liver impairment and in patients taking digoxin or beta blockers

Direct renin inhibitors (like aliskiren)

Bind tightly with renin and thereby inhibit cleavage of angiotensinogen into angiotensin I. This action suppresses the entire RAAS. Like ACE inhibitors and ARBs: -Cause vasodilation -Suppress aldosterone release -Promote excretion of sodium and water -Reduce BP -Cause birth defects and angioedema

Rivaroxaban (Xarelto)

Binds directly with factor Xa to cause inactivation Uses Prevention of DVT and PE after knee or hip replacement surgery Prevention of stroke in patients with a-fib Treatment of DVT and PE unrelated to ortho surgery Advantages: rapid onset, fixed dosage, no blood tests needed, less bleeding and hemorrhagic stroke, few drug-food interactions

Angiotensin II receptor blockers

Block access of angiotensin II Block actions of angiotensin II in blood vessels, the adrenals, and all other tissues Prevent angiotensin II from inducing pathologic changes in cardiac structure Reduce excretion of potassium Similar to ACE inhibitors in that they: -Cause dilation of arterioles and veins -Suppress aldosterone release -Increase renal excretion of sodium and water -Reduce BP -Cause birth defects and angioedema Different from ACE inhibitors in that they: -Do not inhibit kinase II -Do not increase levels of bradykinin -Have a lower incidence of hyperkalemia -Have a lower incidence of cough

Physiology of orthostatic hypotension

Blockade of alpha receptors on veins Reduced muscle tone in the venous wall Upon standing, blood pools in veins Return of blood to heart is reduced Cardiac output decreased: BP drops

Actions of diltiazem

Blocks calcium channels in heart and blood vessels (similar to verapamil) Lowers BP Arteriolar dilation Direct suppressant/reflex cardiac stimulation → little net effect on the heart

Mechanism of action of guanfacine

Both the book and the PPT talk about guanfacine and not guanethidine? Very similar to clonidine

Side effects of verapamil

CONSTIPATION occurs frequently (d/t blockade of calcium channels in smooth muscle of intestine) Dizziness, facial flushing, edema of ankles/feet, headache, gingival hyperplasia (d/t vasodilation) Heart block Drug interactions: digoxin, beta-adrenergic blocking agents

Vaughan Williams Class IV

Calcium channel blockers Same effect as beta blockade Verapamil, diltiazem

Briefly describe the calcium channel and the relationships between intracellular and extracellular calcium concentrations as they affect smooth and cardiac muscle contractile function.

Calcium channels are gated pores in the cytoplasmic membrane that regulate calcium entry into cells In blood vessels, calcium entry causes vasoconstriction, and hence calcium channel blockade causes vasodilation In the heart, calcium entry increases HR, AV conduction, and myocardial contractility, so calcium channel blockade has the opposite effects In the heart, calcium channels are coupled to beta 1 receptors, activation of which enhances calcium entry. As a result, calcium channel blockade and beta blockade have identical effects on cardiac function In vascular smooth muscle, calcium channels regulate contraction. When action potential travels down the surface of a smooth muscle cell, calcium channels open and calcium ions flow inwards, thereby initiating the contractile process. If calcium channels are blocked, contraction will be prevented and vasodilation will result. At therapeutic doses, CCBs act selectively on peripheral arteries and arterioles of the heart and have no significant effect on veins In cardiac muscle, calcium entry has a positive inotropic effect -- increases force of contraction

Prototype: antidysrhythmic drugs

Class 1: sodium channel blockers -- quinidine, lidocaine Class II: beta blockers -- propranolol Class III: drugs that delay repolarization -- amiodarone Class IV: calcium channel blockers -- verapamil Others: adenosine, digoxin

Expected reaction to beta 2 activation

Decrease BP (vasodilate)

Adverse effects of alpha1 blockade

Detrimental effects result from the blockade of alpha1 receptors Receptor effects from alpha2 receptors are minor Orthostatic hypotension Reflex tachycardia Nasal congestion Inhibition of ejaculation Sodium retention and increased blood volume Reduced BP promotes renal retention of sodium and water Usually combined with diuretic when used for HTN ***Most significant adverse effect associated with alpha2 blockade: potentiation of reflex tachycardia**

State the main direct and indirect cardiac contractile and electrophysiologic effects of digoxin and explain the relationship between them and the serum potassium level.

Digoxin effects Positive inotropic action on the heart Increases force of ventricular contraction Increases myocardial contractility Relationship of potassium to inotropic action Potassium levels must be kept in normal physiologic range Hemodynamic benefits Increased CO Decreased sympathetic tone Increased urine production Decreased renin release

Direct effects of verapamil on heart and blood vessels

Direct effects on heart and blood vessels 1. Blockade at peripheral arterioles → reduces arterial pressure 2. Blockade at arteries and arterioles of heart → increases coronary perfusion 3. Blockade at SA node → reduces heart rate 4. Blockade at AV node *most important* → decreases AV nodal conduction 5. Blockade in the myocardium → decreases force of contraction

Automaticity related to dysrhythmias

Disturbances of automaticity can occur in any part of the heart Cells normally capable of automaticity (cells of SA node, AV node, and His-Purkinje system) can produce dysrhythmias if their normal rate of discharge changes In addition, dysrhythmias can be produced if tissues that do not normally express automaticity (atrial and ventricular muscle) develop spontaneous phase 4 depolarization Altered automaticity in the SA node can produce tachycardia or bradycardia Excessive discharge of sympathetic neuron that innervate SA node can augment automaticity to such a degree that sinus tachycardia results Excessive vagal (parasympathetic) discharge can suppress automaticity to such a degree that sinus brady results Increased automaticity of Purkinje fibers is a common cause of dysrhythmias (caused by excessive stimulation by sympathetic nervous system)

Drug interactions with digoxin

Diuretics + digoxin = potassium loss and increased risk of digoxin-induced dysrhythmias Beta blockers/verapamil/diltiazem + digoxin = decreased contractility of heart Sympathomimetics + digoxin = increased contractility and HR Cholestyramine/kaolin-pectin/metoclopramide/neomycin/sulfasalazine + digoxin = decreased digoxin levels by decreasing digoxin absorption or bioavailability Aminoglycosides/antacids/colestipol/azithromycin/clarithromycin/azithromycin/omeprazole/tetracycline + digoxin = increased digoxin levels by increasing digoxin absorption or bioavailability Alprazolam/amiodarone/atorvastatin/captopril/diltiazem/nifedipine/nitrendipine/propafenone/quinidine/verapamil + digoxin = increased digoxin levels by decreasing excretion of digoxin, altering distribution of digoxin, or both

Other antidysrhythmic drugs

Don't fit into 4 major groups Both drugs suppress dysrhythmias by decreasing conduction through AV node and reducing automaticity in SA node Adenosine, digoxin

Drug therapy and non-drug therapy for stable angina

Drug therapy -Organic nitrates: nitroglycerin (vasodilator) acts directly on vascular smooth muscle; decreases oxygen demand -Beta blockers -Calcium channel blockers -Ranolazine can be combined with these for added benefit -Note: drugs provide symptom relief but don't treat underlying cause -To reduce the risk of MI, patients should receive an antiplatelet drug unless it's contraindicated Non-drug therapy -Avoid factors that can precipitate angina -Reduce risk factors: smoking, HTN, hyperlipidemia, sedentary lifestyle

Variant angina - drug therapy

Drug therapy: -Calcium channel blockers -Organic nitrates: nitroglycerin relaxes or prevents spasm in coronary arteries, increases oxygen supply, does not reduce oxygen demand -Both CCBs and organic nitrates relax coronary artery spasm -(Beta blockers and ranolazine not effective with variant asthma) -Therapy is symptomatic only

Prototype: anticoagulants

Drugs that activate antithrombin: heparin, enoxaparin Vitamin K agonist: warfarin Direct thrombin inhibitors: dabigatran Direct factor Xa inhibitors: rivaroxaban, apixaban

Anticoagulants

Drugs that activate antithrombin; they disrupt the coagulation cascade, thereby suppressing the production of fibrin Warfarin inhibits the synthesis of clotting factors (factor X and thrombin), and all other anticoagulants inhibit the activity of clotting factors Prototype drugs Drugs that activate antithrombin (Heparin, enoxaparin) Vitamin K antagonist (warfarin) Direct thrombin inhibitors (dabigatran) Direct factor Xa inhibitors (rivaroxaban, apixaban)

Explain how reducing afterload and preload can help a patient with hypertension or heart failure

Drugs that dilate resistance vessels (arterioles) cause a decrease in cardiac afterload Drugs that dilate capacitance vessels (veins) reduce the force with which blood is returned to the heart, thus reducing preload

State the cardiac and other (noncardiac/extracardiac) signs and symptoms consistent with digoxin toxicity.

Dysrhythmias are the most serious adverse effect of digoxin Non-cardiac adverse effects: anorexia, nausea, vomiting, fatigue, visual disturbances (blurred vision, yellow tinge to vision, halos around dark objects)

Explain the practical clinical implications of classifying some adrenergic blockers as "cardioselective" and others as having intrinsic sympathomimetic activity.

Either block 1 and 2 or just 2 Beta blockers can be divided into three groups: First generation agents: nonselective beta blockers, such as propranolol, which block 1 and 2 Second-generation agents: cardioselective beta blockers, such as metoprolol, which block beta1 receptors only at usual doses Third generation agents: vasodilating beta blockers, which may be cardioselective or nonselective These can be used to avoid detrimental effects in patients with certain conditions -- cardioselective beta blockers are preferred for patients with asthma or DM

Unfractionated heparin (general info, uses, adverse effects, contraindications, antidote, labs)

Enhances antithrombin Rapid action -- administered by injection (IV, subq) only Uses: Preferred anticoagulant during pregnancy, PE, stroke evolving, massive DVT, open heart surgery, renal dialysis, low-dose therapy post-op, DIC, adjunct to thrombolytic therapy Adverse effects: hemorrhage, thrombocytopenia, hypersensitivity reactions Contraindications: thrombocytopenia; uncontrollable bleeding; during and immediately after surgery of eye, brain, or spinal cord Antidote: protamine sulfate Must monitor aPTT

Therapeutic uses of alpha blockers

Essential HTN (cause vasodilation) Relief of toxicity alpha 1 agonists Overdose of alpha-adrenergic agonist (like epi) HTN due to excessive activation of alpha1 receptors on blood vessels Reversal: alpha-blocking agent Extravasated necrosis: infiltrate the region with phentolamine (an alpha-adrenergic antagonist) Blocks vasoconstriction and prevents injury BPH Pheochromocytoma Principal cause of hypertension is usually activation of alpha1 receptors but beta1 receptors can also contribute Raynaud's disease

Dihydropyridines

Ex: nifedipine, nicardipine, amlodipine, isradipine, felodipine, nimodipine, nisoldipine, clevidipine Agents that act mainly on vascular smooth muscle Significant blockade of calcium channels in blood vessels, minimal blockade of calcium channels in heart Seven other dihydropyridines available are similar to nifedipine

Adverse effects of nitroprusside

Excessive hypotension Cyanide poisoning Thiocyanate toxicity

Expected effects and pre-existing conditions that require extra caution with thiazides

Expected effects -Indicated for hypertension and edema Pre-existing conditions that require extra caution -CV disease -Renal impairment -DM -Gout -Patients taking digoxin, lithium, or antihypertensive drugs

Diuretics and HF

First-line drugs for all patients with signs of volume overload By reducing blood volume, these drugs can decrease venous pressure, arterial pressure (afterload), pulmonary edema, peripheral edema, and cardiac dilation For the most part, benefits of diuretics are limited to symptom reduction First-line in patients with signs of fluid overload Limited to symptom reduction Thiazide diuretics - moderate diuresis Principal adverse effect: hypokalemia, risk of dysrhythmias Loop diuretics - profound diuresis Work when GFR is low Adverse effects: hypokalemia, increased risk of digoxin toxicity, hypotension due to excessive volume reduction Potassium-sparing diuretics - scant diuresis Principal adverse effect: hyperkalemia

Explain the blood pressure control gains to be expected by progressively increasing the dosage of one antihypertensive drug rather than adding drugs in other classes to the initial agent.

For each drug in the regimen, dosage should be low initially and then gradually increased For most people with chronic HTN, the disease poses no immediate threat When BP is reduced slowly,, baroreceptors gradually reset to the new lower pressure,and as a result, sympathetic reflexes offer less resistance to the hypotensive effects of therapy Higher doses = higher likelihood of adverse effects

Unstable angina - treatment

Goal: reduce pain and prevent progression to MI/death All patients should be hospitalized Acute management consists of anti-ischemic therapy combined with antiplatelet and anticoagulation therapy ANTI-ISCHEMIC therapy Nitroglycerin: 3 sublingual doses every 5 min, followed by IV therapy if persistent ischemia or HTN occurs Beta blocker: give first dose IV is chest pain is ongoing Supplemental oxygen IV morphine ACE inhibitor ANTIPLATELET therapy Aspirin (indefinitely) Clopidogrel Abciximab Eptifibatide or tirofiban ANTIGCOAGULANT therapy Subq LMW heparin, direct thrombin inhibitors, factor Xa inhibitors, or unfractionated heparin

Adverse effects and drug interactions of amiloride

Remember: this is a potassium-sparing diuretic Adverse effects: -Hyperkalemia Drug interactions -ACE inhibitors -Other drugs that cause hyperkalemia

Recommended drug classes for treatment of HTN in patients with HF, recurrent strokes, CAD, post-MI, DM, CKD

Heart failure: ACE inhibitor, aldosterone antagonist, ARB, beta blocker, CCB, diuretic Recurrent stroke prevention: ACE inhibitor, diuretic High risk of CAD: ACE inhibitor, beta blocker, CCB, diuretic Post-MI: ACE inhibitor, aldosterone agonist, beta blocker Diabetes: ACE inhibitor, ARB, beta blocker, CCB, diuretic -Remember that beta blockers can suppress glycogenolysis and mask early signs of hyperglycemia (use with caution) Chronic kidney disease: ACE inhibitor, ARB -Avoid potassium-sparing diuretics

Some review of clotting, etc.

Hemostasis is the physiologic process by which bleeding is stopped -- occurs in 2 stages: formation of a platelet plug, then reinforcement of the platelet plug with fibrin Fibrin is produced by 2 pathways -- the contact activation pathway (intrinsic pathway) and the tissue factor pathway (extrinsic pathway) -- that converge at clotting factor Xa,, which catalyzes formation of thrombin, which in turn catalyzes formation of fibrin As healing of an injured vessel proceeds, removal of the clot is eventually necessary The body accomplishes this with plasmin, an enzymes that degrades the fibrin meshwork of the lcot Plasmin is produced through the activation of its precursor, plasminogen The fibrinolynic drugs (like alteplase) act by promoting conversion of plasminogen to plasmin

LMW heparin (general info, uses, adverse effects, contraindications, antidote)

Heparin preparations composed of molecules that are shorter than those found in unfractionated heparin Therapeutic uses: prevention of DVT post-op (especially hip and knee replacements), treatment of established DVT, prevention of ischemic complications (patients with unstable angina, non-Q wave MI, and STEMI) Administered subq Dosage based on body weight Antidote: protamine sulfate Can be given at home (no need for monitoring bleeding times) Adverse effects: bleeding (but less than with unfractionated hep), immune-mediated thrombocytopenia, severe neurologic injury for patients undergoing spinal puncture

Vasodilators in patients with HF

IV vasodilators for acute care Principal adverse effects of nitroglycerin: hypotension, reflex tachycardia Principal adverse effect of sodium nitroprusside: profound hypotension Principal adverse effect of nesiritide: symptomatic hypotension

Explain the cardiac (beta 1) effects of adrenergic agonists.

Increase HR, increase contractility, increase cardiac conduction, increase velocity (chronotropy)

Clinical consequences of activation of beta 1 receptors

Increase HR, increase squeeze Positive inotrope

Expected effects and pre-existing conditions that require extra caution with loop diuretics

Indicated in patients with 1)pulmonary edema associated with CHF, 2) edema of hepatic, cardiac, or renal origin that has been unresponsive to less effective diuretics, 3) hypertension that cannot be controlled with thiazide and potassium-sparing diuretics, and 4) patients who need diuretic therapy but have low renal blood flow Pre-existing conditions that require extra caution -CV disease -Renal impairment -DM -Gout -Pregnancy -Patients on digoxin, lithium, ototoxic drugs (I feel like that will be a test question), NSAIDs, or antihypertensive drugs

Indirect and net effects of verapamil

Indirect effects Reflex hemodynamic effects Baroreceptor reflex Net effects Little or no net effect on cardiac performance Vasodilation accompanied by reduced arterial pressure and increased coronary perfusion

Antiplatelets

Inhibit platelet aggregation Thrombolytics: promote lysis of fibrin, causing dissolution of thrombi Prototype drugs Antiplatelet drugs (aspirin, clopidogrel, abciximab) Thrombolytic drugs (streptokinase, alteplase)

Direct effects of nifedipine

Limited to blockade of calcium channels in vascular smooth muscle (No direct suppressant effects on automaticity, AV conduction, or contractile force)

Which diuretic should you prescribe if GFR is low?

Loop diuretics (in contrast to thiazide diuretics) are effective even when GFR is low

__________________ are used to treat hypertension and edema associated with heart failure, cirrhosis, and kidney disease

Loop diuretics and thiazides

Which type of diuretic produces the greatest diuresis?

Loop diuretics block sodium and chloride in the Loop of Henle (and produce the greatest diuresis)

Some adverse effects to think about

Loops can cause hearing loss; thiazides do not cause hearing loss Potassium-sparing diuretics can produce hyperkalemia -- use with caution in combo with others and also in combo with potassium supplements Loops not recommended in pregnancy

Prototype: Angiotensin II-receptor blocker

Losartan

Net effect of nifedipine

Lowered BP Increased HR Increased contractile force

Indirect effects of nifedipine

Lowered BP activates baroreceptor reflex Primarily with immediate release (not sustained release) Vasodilation by blocking calcium channels

Identify individuals who should carry an EpiPen, when they should use it, how dosage should be calculated, and how it should be stored and replaced.

Not sure about dosage calculation because it's a preloaded injection... Need to be stored at room temp in a dark place (sensitive to heat and lights)

Discuss the drugs for hypertensive emergencies.

Major drugs reduce BP by causing vasodilation, and all are given IV Sodium nitroprusside -Drug of choice for hypertensive emergencies -Vasodilator that relaxes smooth muscle of arterioles and veins Fenoldopam -Lowers BP by activating dopamine 1 receptors on arterioles to cause vasodilation Labetalol -Blocks alpha- and beta-adrenergic receptors BP is reduced by arteriolar dilation secondary to alpha blockade -Beta blockade prevents reflex tachycardia (therefore probably safe for patients with angina or MI) Diazoxide Clevidipine -CCB with an ultrashort half-life (about a minute)

Statins (quicker review of mechanism of action, clinical indications, side effects)

Mechanism of action: increase the number of LDL receptors on hepatocytes Clinical indications: hypercholesterolemia, primary and secondary prevention of CV events, primary prevention of CV events in people with normal LDL levels, post-MI therapy, diabetes Side effects: myopathy/rhabdo, hepatotoxicity, new onset DM, memory loss, cataracts, headache, GI disturbances and rash

Niacin (mechanism of action, clinical indications, side effects)

Mechanism of action: not in PPT or text Reduces LDL and TG levels Increases HDL levels more effectively than any other drug Effect on plasma lipoproteins Clinical indications: not in PPT or text Side effects: skin (flushing, itching), GI disturbances, hepatotoxicity, hyperglycemia, gouty arthritis

Nitroglycerin (for tx of angina) -- mechanism of action, adverse effects

Mechanisms of action -Acts on smooth muscle to promote vasodilation in stable angina -Acts to decrease spasm in variant angina Adverse effects -Headache -Orthostatic hypotension -Reflex tachycardia -Tolerance can develop rapidly

Unstable angina -- patho

Medical emergency Symptoms result from severe CAD complicated by vasospasm, platelet aggregation, and transient coronary thrombo/emboli Patient presents with either symptoms of angina at rest, new-onset exertional angina, or intensification of existing angina Greater risk of death than stable angina, but smaller risk of death than MI

Drugs of choice for treating chronic HTN of pregnancy

Methyldopa and labetalol -ACE inhibitors, ARBs, and DRIs are contraindicated during pregnancy -Most other antihypertensives can be continued during pregnancy

General info to remember about diuretics

Most diuretics block active reabsorption of sodium and chloride, thereby preventing passive reabsorption of water The amount of diuresis produced is directly related to the amount of sodium and chloride reabsorption blocked Drugs that act early in the nephron block the greatest amount of solute reabsorption and produce the greatest diuresis

Prototype: vasodilators

Nitroprusside

Know when cardioselective drugs should/should not be prescribed.

Nonselective beta blockers can suppress glycogenolysis and can suppress the early warning signs of falling glucose level (tachycardia, tremors and perspiration) -- this can be detrimental in patients with DM

Adverse effects of beta blockade

Nonselective beta-adrenergic blocking agents produce a broader spectrum of adverse effects than the cardioselective beta-adrenergic antagonists Bradycardia Reduced CO Precipitation of heart failure AV heart block Rebound cardiac excitation Bronchoconstriction Contraindicated in people with asthma or severe constrictive lung disease Hypoglycemia from inhibition of glycogenolysis

Prototype: drugs for angina pectoris

Organic nitrates: nitroglycerin Beta blockers: metoprolol, propranolol Calcium channel blockers: nifedipine, verapamil Drug that increases myocardial efficiency: ranolazine

Stable angina: patho and treatment strategy

PATHO -Triggered most often by an increase in physical activity -Emotional excitement, large meals, and cold exposure may precipitate an attack -Underlying cause: CAD TREATMENT STRATEGY -Goal of therapy: reduce intensity and frequency of attacks -2 possible remedies: increase cardiac oxygen supply or decrease oxygen demand -The first isn't really possible because the underlying cause of stable angina is occlusion of the coronary arteries -Oxygen demand can be reduced with drugs that decrease HR, contractility, afterload, and preload

Contraindications of ACE inhibitors

Patients with bilateral RENAL ARTERY STENOSIS or stenosis in the artery to a single remaining kidney (because they can cause renal failure) Can cause FETAL INJURY -- women who become pregnant while using ACE inhibitors should discontinue treatment as soon as possible ANGIOEDEMA is a potentially fatal reaction that occurs in 1% of patients -- should be discontinued and never used again if angioedema develops Other adverse effects (not contraindications) include -Hyperkalemia -First dose hypotension -Cough -Neutropenia

Vaughan Williams Class III

Potassium channel blockers Block potassium channels and delay repolarization of fast potentials (Drugs that delay repolarization): amiodarone, dronedarone, sotalol, dofetilide, ibutilide

Direct Factor Xa inhibitors

Produce selective inhibition of Xa rivaroxaban and apixaban

Beta blockers in tx of angina

Propranolol, metoprolol Decrease oxygen demand Adverse effects -Bradycardia -Decreased AV conduction -Reduction of contractility -Asthmatic effects -Use with caution in patients with diabetes -Insomnia -Depression -Bizarre dreams -Sexual dysfunction

Contraindications of direct renin inhibitors

Pts with hyperkalemia Hx of angioedema 2nd and 3rd trimesters of pregnancy

Drugs that inhibit the RAAS in patients with HF

RAAS plays an important role in cardiac remodeling and the hemodynamic changes that occur in response to reduced CO Agents that inhibit the RAAS can be highly beneficial 5 groups: ACE inhibitors, ARBs, angiotensin receptor neprilysin inhibitors, DRIs, and aldosterone antagonists ACE inhibitor benefits: arteriolar dilation, venous dilation, suppression of aldosterone release, and favorable impact on cardiac remodeling ACE inhibitor limitations: can cause hypotension, hyperkalemia and angioedema; can cause renal failure in patients with renal artery stenosis; can cause fetal injury ARBs have shown benefits in clinical trials: improvement of LV ejection fraction, reduction of HF symptoms, increased exercise tolerance, decreased hospitalization, enhanced quality of life and reduction in mortality Aldosterone antagonists have benefits -- current studies recommend adding them to standard HF therapy in patients with moderately severe or severe symptoms DRIs have similar benefits to ACE inhibitors and ARBs, but have not yet been approved for HF treatment

Clinical consequences of activation of alpha1 receptors

Raise BP (vasoconstrict) Hemostasis (stops bleeding with vasoconstriction) Nasal decongestion (mucosal vasoconstriction) Adjunct to local anesthetic (delays absorption) Mydriasis (dilation of radial muscle of iris)

Discuss adding drugs to the regimen to treat HTN

Rationale for drug selection -When using 2 or more drugs to treat HTN, each drug should come from a different class (and therefore have a different mechanism of action) Benefits of multidrug therapy -Targeting BP control at several sites is likely to be more effective than targeting at one site -Lower dosages can be used of each drug when you combine drugs -One agent can also offset the adverse effects of another (if a vasodilator is combined with a beta blocker, reflex tachycardia is minimal; using a vasodilator alone, reflex tachycardia is likely)

Explain the factors that lead to and the characteristics of the "rebound" phenomenon associated with sudden discontinuation of clonidine.

Rebound hypertension happens with abrupt clonidine withdrawal (rare but dangerous) Caused by overactivity of the SNS Accompanied by nervousness, tachycardia and sweating Can be avoided by withdrawing slowly (over 2-4 days)

Effects of statins

Reduction of LDL cholesterol Elevation of HDL cholesterol Reduction of triglyceride levels Reduce mortality Non-lipid beneficial cardiovascular actions Promote plaque stability Reduce the risk for CV events Increased bone formation

Clinical consequences of activation of alpha2-adrenergic receptors

Reduction of sympathetic outflow to the heart and blood vessels Relief of severe pain

Adverse effects of hydralazine

Reflex tachycardia Increased blood volume Lupus-like syndrome Headache, dizziness, weakness, and fatigue Drug interactions -Other hypertensive agents -Avoid excessive hypotension -Can be combined with a beta blocker to protect against reflex tachycardia and with diuretics to prevent sodium and water retention and expansion of blood volume

Adverse effects of minoxidil

Reflex tachycardia Sodium and water retention Hypertrichosis Pericardial effusion

Side effects of nifedipine

Reflex tachycardia -- increases cardiac oxygen demand and can increase pain in patients with angina Can be combined with a beta blocker like metoprolol to prevent reflex tachycardia Flushing, dizziness, headache, peripheral edema, gingival hyperplasia all d/t vasodilation Chronic eczematous rash in older patients Immediate release has been associated with increased mortality in patients with MI and unstable angina Other rapid-acting calcium channel blockers also associated Use with great caution Note: not likely to exacerbate AV heart block, heart failure, etc. like verapamil

Identify the desired effects when a therapeutic dose of epinephrine is given for anaphylaxis and explain the actions of the drug that earn it the label "drug of choice" for anaphylaxis.

Remember that anaphylaxis causes bronchoconstriction, hypotension (from widespread vasodilation), and edema of the glottis Epi causes bronchial dilation, raises BP Epi activates alpha1, beta1 and beta2 adrenergic receptors and can therefore reverse the most severe manifestations of an anaphylactic reaction Activation of beta1 receptors increases CO, helps to elevate BP BP also goes up because of activation of alpha1 causing vasoconstriction; vasoconstriction also suppresses epiglottal edema Activation of beta1 receptors counteracts bronchoconstriction Epi works better than antihistamines because histamine is only one of several contributors to the reaction

Adverse effects of triamterene

Remember: this is a potassium-sparing diuretic Adverse effects -Hyperkalemia -Leg cramps -Vomiting -Dizziness -Blood dyscrasias (rare)

Adverse effects and drug interactions with spironolactone

Remember: this is a potassium-sparing diuretic Adverse effects -Hyperkalemia -Benign and malignant tumors -Endocrine effects (gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of voice) Drug interactions -Thiazide and loop diuretics -Agents that raise potassium levels

Adverse effects of mannitol

Remember: this is an osmotic diuretic Adverse effects -Edema -Headache -Nausea -Vomiting -Electrolyte imbalance

Compare and contrast the general sites and mechanisms of action of reserpine, clonidine, and methyldopa with those of drugs that block adrenergic receptors (e.g., propranolol, phentolamine).

Reserpine, clonidine, and methyldopa act in the CNS -- do so by mechanisms other than direct receptor blockade I think propranolol works on receptors on veins Clonidine and methyldopa act on receptors in the brainstem

Rhabdo (identify the main class of drugs associated with it, its clinical consequences, and factors that increase the risk for this syndrome)

Rhabdo is a rare and potentially fatal adverse effect of statins Muscle disintegration of dissolution Release of muscle components lead to marked elevations of blood CK (greater than 10x upper limit of normal) and elevations of free myoglobin High levels of CK may cause renal impairment Increased risk: small body frame, advanced age, frailty, multisystem disease (like chronic renal insufficiency, especially associated with DM), hypothyroidism,use of statins in high doses, low vitamin D and coenzyme Q levels, concurrent use of fibrates, and the use of drugs that can raise statin levels

Therapeutic application of beta1 activation

SHOCK Profound hypotension and greatly reduced tissue perfusion Primary goal of treatment is to maintain blood flow to vital organs Beta2 stimulation increases heart rate and force of contraction Increases cardiac output Improves tissue perfusion HEART FAILURE Increases force of contraction AV heart block Enhances impulse conduction through AV nodes Only temporary treatment -- long-term management is pacemaker CARDIAC ARREST Can initiate contraction in a heart that has stopped beating Drugs are not preferred treatment Initial management = CPR, external pacing, or defibrillation Also identification and treatment of underlying cause Adverse effects of beta1 activation DYSRHYTHMIAS

Apixaban (Eliquis)

Selective inhibition of factor Xa Inhibits free and clot-bound factor Xa, as well as prothrombinase activity Use: prevention of stroke and systemic embolis in patients with nonvalvular a-fib Advantages: rapid onset, fixed dosage, no blood tests needed, less bleeding and hemorrhagic stroke, few drug-food interactions

Side effects of diltiazem

Similar to verapamil, but less constipation Dizziness, flushing, headache, edema, of ankles and feet (all d/t vasodilation) Exacerbates sick sinus syndrome, bradycardia, heart failure, second-degree or third-degree heart block Drug interactions: digoxin, beta-adrenergic blocking agents

Vaughan Williams Class I

Sodium channel blockers These drugs slow impulse conduction in the atria, ventricles and His-Purkinje system IA: quinidine, procainamide, disopyramide IB: lidocaine, phenytoin, mexiletine IC: flecainide, propafenone

Pharmacologic effects with vasodilation

Some vasodilators are selective for arterioles (hydralazine), some are selective for veins (nitroglycerin), and some dilate both types (prazosin) Drugs that dilate arterioles reduce cardiac afterload and can thereby reduce cardiac work while increasing cardiac output and tissue perfusion Drugs that dilate veins reduce cardiac preload and can thereby reduce cardiac work, cardiac output, and tissue perfusion

Adverse effects of statins

Statins can cause liver damage -- tests of liver function should be done at baseline and as clinically indicated thereafter Statins can cause myopathy -- patients who experience unusual muscle pain, soreness, tenderness, and/or weakness should inform their provider Creatinine kinase (a marker for muscle injury) should be measured at baseline, before starting the drug, and whenever signs or symptoms that could be due to myositis or myopathy develop Statins should not be used in pregnancy Common adverse effects -Headache -Rash -GI disturbances Rare -Myopathy/rhabdo -Hepatotoxicity -New-onset diabetes -Cataracts

Mechanism of action for statins

Statins reduce LDL cholesterol levels by increasing the number of LDL receptors on hepatocytes, thereby enabling hepatocytes to remove more LDLs from the blood The process by which LDL receptor number is increased begins with inhibition of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis Four statins (atorvastatin, fluvastatin, lovastatin, and simvastatin) are metabolized by CYP3A4, and hence their levels can be increased by CYP3A4 inhibitors (e/g/, cyclosporine, erythromycin, ketoconazole, ritonavir) Adverse effects

Discuss routine drug therapy for management of STEMI.

Supplemental oxygen Aspirin (not NSAIDs) Morphine Beta blockers Nitroglycerin

Inotropic agents in patients with HF

Sympathomimetics Dopamine Activates beta1-adrenergic receptors in the heart, kidney, and blood vessels Increases HR, dilates renal blood vessels, activates alpha1 receptors Dobutamine Selective activation of beta1-adrenergic receptors Phosphodiesterase inhibitors (milrinone) Increases myocardial contractility and promotes vasodilation Reserved for patients with severe reduction in CO resulting in decreased organ perfusion Limitations: can cause arrhythmias and myocardial ischemia

State how changes in the serum potassium level influence the effects of digoxin and the likely impact of hypokalemia or hyperkalemia on therapy with a cardiac glycoside.

The most common cause of dysrhythmias in patients receiving digoxin is hypokalemia secondary to the use of diuretics If potassium level is low, potassium should be given PO or IV Potassium displaces digoxin from Na/K ATPase and thereby helps reverse toxicity If potassium levels are high or if AV block is present, additional potassium given can cause complete AV block

What are the preferred drugs for initial therapy of uncomplicated hypertension?

Thiazide diuretics Thiazide diuretics and loop diuretics reduce BP by reducing blood volume and reducing arterial resistance Loop diuretics should be reserved or patients who need greater diuresis than can be achieved with thiazides and/or in patients with low GFR

____________ are helpful for mobilizing edema in hepatic and renal disease

Thiazides

Diuretics with heart failure

Thiazides are preferred drugs for mobilizing edema associated with mild to moderate heart failure; potassium-sparing diuretics decrease mortality in severe HF

Name the concepts associated with secondary prevention of STEMI.

To lower the risk of a second MI, all patients should decrease CV risk factors (smoking, hypercholersterolemia, HTN, DM), exercise for 30 minutes at least 3-4 days per week, undergo long-term therapy with 4 drugs: beta blocker, ACE inhibitor or ARB, antiplatelet or warfarin, and a statin

Adverse effects of beta2 activation

Tremor

Anticoagulation in pregnant women

Unfractionated heparin is the preferred therapy in pregnant women LMW heparin also does not cross the placenta Warfarin is contraindicated d/t fetal hemorrhage and teratogenesis Thrombolytics should be used with great caution in pregnancy

Describe how the use of diuretics as an adjunct to digoxin can be considered beneficial and/or dangerous.

Use of thiazide diuretics increases risk of digoxin-induced dysrhythmias Use of loop diuretics increases risk of digoxin toxicity In patients with HF, potassium-sparing diuretics are used to counteract potassium loss caused by thiazide and loop diuretics, thereby lowering the risk of digoxin-induced dysrhythmias

Adverse effects of activation of alpha 1 receptors

Vasoconstriction can cause hypertension, bradycardia, and necrosis

nifedipine actions/basics

Vasodilation by blocking calcium channels Cannot be used to treat dysrhythmias Less likely than verapamil to exacerbate pre-existing cardiac disorders

Sites of action of verapamil and diltiazem

Verapamil and diltiazem act on vascular smooth muscle and the heart and blood vessels, especially arterioles Dihydropyridines (like nifedipine) act mainly on vascular smooth muscle and blood vessels, especially arterioles

Calcium channel blockers (for tx of angina) - mechanism of action, adverse effects

Verapamil, diltiazem, nifedipine Block calcium channels in vascular smooth muscle Used for stable and variant angina Adverse effects -Dilation of peripheral arterioles -Reflex tachycardia -Hypotension -Because of their suppressant effects on the heart, use with caution in patients taking beta blockers and in patients with bradycardia, heart failure, and AV block

Warfarin (general info, adverse effects, antidote, drug interactions)

Vitamin K antagonist Oral anticoagulant with delayed onset (not useful in emergencies) Blocks biosynthesis of factors VII, IX, and X, and prothrombin Long-term prophylaxis of thrombosis Prevention of venous thrombosis and associated PE Prevention of thromboembolism (in patients with prosthetic heart valves) Prevention of thrombosis during atrial fibrillation Monitor PT and INR Adverse effects: hemorrhage, fetal hemorrhage, teratogenesis Antidote: vitamin K Remember dietary sources of vitamin K are mayonnaise, canola oil, soybean oil, and green leafy vegetables Drug interactions Drugs that increase or decrease anticoagulant effects Drugs that promote bleeding Heparin Aspirin Acetaminophen

Beta blockers in patients with HF

With careful control of doses (to avoid reduced contractility in a heart that is already compromised and failing), beta blockers can improve patient status When added to conventional therapy, some beta blockers can improve LV ejection fraction, increase exercise tolerance, slow progression of HF, reduce the need for hospitalization, and prolong survival Protect from excessive sympathetic stimulation Protect against dysrhythmias Limitations: fluid retention, worsening of HF, fatigue, hypotension, bradycardia, heart block

Prototype: direct renin inhibitor

aliskiren

Which receptor(s) is/are activated by phenylephrine?

alpha 1

Which receptor(s) is/are activated by norepi?

alpha 1, alpha 2, beta 1

Which receptor(s) is/are activated by epi?

alpha 1, alpha 2, beta 1, beta 2

Ivabradine in patients with HF

an be used in patients who have a contraindication to beta blocker use

Prototype: antiplatelet drugs

aspirin clopidogrel abciximab

Which receptor(s) is/are activated by dobutamine?

beta 1

Prototype: ACE inhibitor

captopril

Mechanism of action of clonidine

causes selective activation of alpha2 receptors in the CNS -- specifically in the brainstem areas associated with autonomic regulation of the CV system By activating these receptors, clonidine reduces sympathetic outflow to blood vessels and to the heart *CENTRALLY acting alpha 2 agonist*

Prototype: centrally acting (alpha 2) adrenergic agonist

clonidine

Hypertensive emergency =

diastolic BP >120 mmHg

Indirect-acting antiadrenegic agents (in general)

drugs that prevent the activation of peripheral adrenergic receptors, but by mechanisms that do not involve direct interaction with peripheral receptors 2 categories: centrally acting alpha2 agonists act within the CNS to reduce the outflow of impulses along sympathetic neurons, and adrenergic neuron-blocking agents act within the terminals of sympathetic neurons to decrease NE release Centrally acting alpha2 agonists

Prototype: adrenergic agonists

ephinephrine

Prototype: aldosterone antagonist

eplerenone

Prototype: loop diuretic

furosemide (Lasix)

Inotropic agents (digoxin) in patients with HF

have positive inotropic action → increase myocardial contractile force and therefore increase CO Can reduce symptoms, but doesn't prolong life

Prototype: thiazide diuretic

hydrochlorothiazide

Prototype: beta-selective adrenergic agonists

isoproterenol

Prototype: selective (beta 1) adrenergic antagonist (beta blocker)

metoprolol (Lopressor)

Prototype: calcium channel blocker -- agents that act mainly on blood vessels

nifedipine

Dosing for statins

once daily in the evening (greatest impact)

All loop diuretics can cause:

ototoxicity, hypovolemia, hypotension, hypokalemia, hyperuricemia, hyperglycemia, and disruption of lipid metabolism

Prototype: selective (alpha 1) adrenergic antagonist (alpha blocker)

prazosin (Minipress)

Prototype: nonselective beta adrenergic antagonist (beta blocker)

propranolol

Prototype: adrenergic neuron-blocking agent

reserpine

Verapamil toxicity

severe hypotension, bradycardia and AV block, ventricular tachydysrhythmias Treated with gastric lavage and activated charcoal

Prototype: potassium-sparing diuretic

spironolactone (Aldactone) triamterene

First drug class for lowering LDL

statins (HMG-CoA reductase inhibitors)

Prototype: thrombolytic drugs

streptokinase alteplase (TPA)

Aspirin

suppresses platelet aggregation Indications -Ischemic stroke (to reduce the risk of death and nonfatal stroke) -TIAs (to reduce the risk of death and nonfatal stroke) -Chronic stable angina (to reduce the risk of MI and sudden death) -Unstable angina (to reduce the combined risk of death and nonfatal MI) -Coronary stenting (to prevent reocclusion) -Acute MI (to reduce the rik of vascular mortality) -Previous MI (to reduce the combined risk of death and nonfatal MI) -Primary prevention of MI (to prevent a firs MI in men and in women ages 65 and older) Dosage is low for preventing CV events, cost is low compared to other prescription drugs Not sure about targets and lab tests

beta1-adrenergic receptors are in:

the cardiac cells

beta2-adrenergic receptors are in:

the vascular and bronchiolar smooth muscle Limited to the lungs and the uterus (but this is contradicted in a later slide...)

alpha1-adrenergic receptors are in:

the vascular smooth muscle

Prototype: calcium channel blocker -- agents that affect the heart and blood vessels

verapamil

Are there any other steps the nurse should take regarding IV administration of mannitol?

•Along with following all the appropriate safety precautions for medication administration, the nurse should use a filter needle to withdraw mannitol from the vial, as well as an in-line filter for IV infusion, to prevent crystals from entering the circulation.

The nurse teaches a patient about benazepril [Lotensin]. Which statement by the patient requires an intervention by the nurse? A."I use NoSalt instead of salt to season foods." B."I eat sweet potatoes once or twice a week." C."I drink 4 ounces of prune juice each morning." D."I like asparagus because it's high in vitamin K."

•Answer: A •Rationale: An adverse effect of angiotensin-converting enzyme (ACE) inhibitors (for example, benazepril) is hyperkalemia. Significant potassium accumulation is usually limited to patients taking potassium supplements, salt substitutes (which contain potassium), or a potassium-sparing diuretic. Patients should be instructed to avoid potassium supplements and potassium-containing salt substitutes unless they are prescribed. Sweet potatoes and prune juice are foods high in potassium; asparagus is high in vitamin K. Foods high in vitamin K are restricted for patients who are prescribed warfarin [Coumadin].

Cholestyramine has been prescribed for a patient. Which instruction should the nurse include in patient teaching? A.Cholestyramine can impair absorption of fat-soluble vitamins. B.Stop taking the drug if you develop constipation. C.Take cholestyramine with other drugs you are prescribed to enhance absorption. D.Do not take the medication if the formula is cloudy after mixing with water.

•Answer: A •Rationale: Cholestyramine is a bile acid sequestrant. Cholestyramine can impair absorption of fat-soluble vitamins (A, D, E, and K); vitamin supplements may be required. Cholestyramine causes constipation; patients should be informed that constipation can be minimized by increasing dietary fiber and fluids. A mild laxative may be used if needed. Instruct patients taking cholestyramine or colestipol to notify the prescriber if constipation becomes bothersome, in which case a switch to colesevelam should be considered. Cholestyramine can bind with other drugs and prevent their absorption. Advise patients to administer other medications 1 hour before or 4 hours after cholestyramine. Cholestyramine powder should be mixed with water, fruit juice, soup, or pulpy fruit (for example, applesauce, crushed pineapple) to reduce the risk of esophageal irritation and impaction. Inform patients that the sequestrants are not water soluble, therefore the mixtures will be cloudy suspensions, not clear solutions.

The health care provider prescribes sustained-release verapamil [Calan SR] to an 82-year-old patient who takes digoxin [Lanoxin] daily. Which action is most appropriate for the nurse to take? A.Monitor the patient's cardiac rhythm continuously. B.Assess the patient for tachycardia and hypertension. C.Maintain the patient on bed rest for 8 to 10 hours. D.Reduce dietary fiber to prevent loose, watery diarrhea.

•Answer: A •Rationale: Digoxin and verapamil suppress impulse conduction through the atrioventricular (AV) node. When these drugs are used concurrently, the risk of AV block is increased. The cardiac rhythm of patients receiving both medications should be monitored closely. The patient should be monitored for bradycardia and hypotension. Bed rest is not indicated. Constipation may occur; increased dietary fiber and fluids are indicated to prevent constipation.

A patient is prescribed lovastatin [Mevacor]. The nurse will teach the patient to take the medication at which time? A.With any meal B.With the evening meal C.1 hour before breakfast D.2 hours after a meal

•Answer: B •Rationale: Lovastatin should be taken with the evening meal to increase absorption. Cholesterol synthesis normally increases during the night; statins are most effective when given in the evening.

The nurse cares for a patient receiving digoxin [Lanoxin]. What indicates to the nurse that treatment with this medication is effective? A.Improved cardiac output B.Reduced exercise tolerance C.Increased body weight Decreased cardiac contractility

•Answer: A •Rationale: Digoxin increases the cardiac output of patients with heart failure; it improves cardiac output, decreases the heart rate, decreases heart size, decreases constriction of arterioles and veins, reverses water retention, decreases blood volume, decreases peripheral and pulmonary edema, decreases weight (by water loss), and improves exercise tolerance.

A patient is started on a dobutamine infusion for the treatment of acute decompensated heart failure. The nurse should assess the patient for the major adverse effect of dobutamine therapy, which is what? A.Supraventricular tachycardia B.Fine hand tremors C.Atrioventricular heart block D.Hyperglycemia

•Answer: A •Rationale: Dobutamine causes the selective activation of beta1-adrenergic receptors, and it is indicated only for the treatment of heart failure. The major adverse effect is tachycardia.

When providing discharge teaching for a patient who has been prescribed furosemide [Lasix], it is most important for the nurse to include which dietary items to prevent adverse effects of furosemide [Lasix] therapy? A. Oranges, spinach, and potatoes B. Baked fish, chicken, and cauliflower C. Tomato juice, skim milk, and cottage cheese D. Oatmeal, cabbage, and bran flakes

•Answer: A •Rationale: Furosemide may have the adverse effect of hypokalemia. Hypokalemia can be reduced by consuming foods that are high in potassium, such as nuts, dried fruits, spinach, citrus fruits, potatoes, and bananas.

A patient with angina pectoris is prescribed sublingual nitroglycerin. Which statement made by the patient indicates understanding of the medication teaching? A."I may experience a headache as a side effect." B."The chest pain should be relieved within 20 minutes." C."I should swallow the tablet and drink a glass of water." D."I should take this medication in the morning before breakfast."

•Answer: A •Rationale: Headache is a common adverse effect of nitroglycerin and is due to vasodilation. If chest pain is not relieved in 5 minutes, the person should dial 911. A sublingual tablet should be placed under the tongue and allowed to dissolve. Sublingual nitroglycerin is used to abort anginal attacks and is not a scheduled medication.

A nurse administers quinidine sulfate to a patient with atrial fibrillation. The nurse should assess the electrocardiogram (ECG) tracing knowing that quinidine sulfate has what effect on the ECG? A.Prolongation of the QT interval B.Prolongation of the PR interval C.Narrowing of the QRS complex D.Tall, peaked T waves

•Answer: A •Rationale: Quinidine sulfate has two pronounced effects on the electrocardiogram (ECG): it widens the QRS complex and prolongs the QT interval.

A patient is receiving an intravenous infusion of heparin to treat a pulmonary embolism. What laboratory value will the nurse monitor to evaluate treatment with this medication? A.Activated partial thromboplastin time (aPTT) B.Prothrombin time (PT) C.Platelet count D.Hemoglobin and hematocrit

•Answer: A •Rationale: The most commonly used laboratory value that monitors the effect of heparin is the activated partial thromboplastin time (aPTT).

The nurse cares for a patient with a digoxin level of 1.9 ng/mL. Which action would be most appropriate for the nurse to take initially? A.Start continuous heart monitoring. B.Check the patient's serum creatinine. C.Administer digoxin as prescribed. D.Give Fab antibody fragments [Digibind].

•Answer: A •Rationale: The optimal therapeutic range for digoxin is 0.5 to 0.8 ng/mL; levels higher than 2 ng/mL usually are associated with toxic symptoms. A priority action is to assess for dysrhythmias; the nurse should immediately initiate continuous heart monitoring. Serum creatinine indicates renal function, and digoxin is eliminated primarily by renal excretion. Renal impairment can lead to toxic accumulation, and the dosage must be reduced if kidney function declines. Digoxin should not be given to a patient suspected of having digoxin toxicity. If a severe digoxin overdose is responsible for dysrhythmias, digoxin levels can be lowered using Fab antibody fragments.

A patient with severe hypertension is prescribed minoxidil. Which medications will the nurse expect to be administered to reduce adverse responses to minoxidil? A.Adenosine [Adenocard] and ticlopidine [Ticlid] B.Furosemide [Lasix] and propranolol [Inderal] C.Digoxin [Lanoxin] and captopril [Capoten] D.Donepezil [Aricept] and clonidine [Catapres]

•Answer: B •Rationale: Minoxidil may cause adverse responses (for example, reflex tachycardia, expansion of blood volume, pericardial effusion). Minoxidil should be used with a beta blocker (for example, propranolol) plus intensive diuretic therapy (for example, furosemide).

The nurse cares for a patient with asthma who uses an albuterol (Ventolin) metered-dose inhaler. The nurse is most concerned if the patient makes which of the following statements? A."The medicine in the inhaler helps me to breathe." B."I can use the inhaler as often as needed." C."My hand starts to shake after I use the inhaler." D. "If the inhaler doesn't work, I should dial 911."

•Answer: B •Rationale: Albuterol can reduce airway resistance in patients with asthma by causing beta2-mediated bronchodilation. If it is administered in large doses, albuterol will lose selectivity; it will activate beta1 receptors as well as beta2 receptors. Accordingly, patients should be warned not to exceed the recommended dosage, because doing so may cause tachycardia by activating beta1 receptors in the heart. Tremor is a common adverse effect of this drug.

The nurse will teach a patient who is prescribed niacin [Niacor] to prevent flushing of the face by doing what? A.Drinking a full glass of water after taking the medication B.Taking 325 mg of aspirin 30 minutes before each dose C.Ingesting a meal before taking the medication D.Increasing dietary fiber before and after each dose

•Answer: B •Rationale: Aspirin reduces flushing by preventing the synthesis of prostaglandins, which mediate the flushing response.

A nurse instructs a patient about signs and symptoms of digoxin toxicity. The nurse determines that teaching is successful if the patient makes which statement? A."If my heart is racing, the dose may be too high." B."I should report any muscle weakness or nausea." C."My doctor should be notified if diarrhea occurs." D."The dose will be reduced if I develop memory loss."

•Answer: B •Rationale: Digoxin toxicity manifests with dysrhythmias, bradycardia, muscles weakness, anorexia, nausea, vomiting, fatigue, and visual disturbances.

After an intramuscular injection of penicillin, a patient develops severe difficulty breathing and a swollen tongue. Which medication should the nurse prepare to administer? A.Dopamine [Inotropin] B.Epinephrine [Adrenalin] C.Norepinephrine [Levophed] D.Pseudoephedrine [Sudafed]

•Answer: B •Rationale: Epinephrine is the drug of choice for patients in anaphylactic shock.

A patient diagnosed with ST-elevation myocardial infarction has been scheduled for an angioplasty. Which medication does the nurse anticipate administering before this procedure? A.Dobutamine [Dobutrex] B.Abciximab [ReoPro] C.Alteplase [Activase] Warfarin [Coumadin]

•Answer: B •Rationale: Glycoprotein IIb/IIIa inhibitors (for example, abciximab) are powerful intravenous antiplatelet drugs that can enhance the benefits of primary percutaneous coronary intervention (PCI). Treatment with abciximab should begin as soon as possible before PCI and should continue for 12 hours afterward.

A patient with heart failure who takes furosemide [Lasix] is diagnosed with bacterial pneumonia. Which medication, if ordered by the physician, should the nurse question? A.Ciprofloxacin [Cipro] B.Gentamicin [Garamycin] C.Amoxicillin [Amoxcil] D.Erythromycin [E-Mycin]

•Answer: B •Rationale: High-ceiling loop diuretics may cause hearing impairment; furosemide may result in deafness that is transient. Because of the risk of hearing loss, caution is needed when high-ceiling diuretics are used in combination with other ototoxic drugs (for example, aminoglycoside antibiotics). Gentamicin is an aminoglycoside. The other antibiotics are safe to administer with furosemide.

A patient is prescribed hydralazine. What is most important for the nurse to teach the patient? A.Precautions for postural hypotension B.Prevention of reflex tachycardia C.High initial dose for slow acetylators D.Recognition of hypertrichosis

•Answer: B •Rationale: Hydralazine is usually combined with a beta blocker to protect against reflex tachycardia. Hydralazine is an arterial vasodilator; postural hypotension is minimal. Hydralazine is inactivated by acetylation, and the ability to acetylate drugs is genetically determined. To avoid hydralazine accumulation, the dosage should be reduced in slow acetylators. Minoxidil commonly causes hypertrichosis, or increased hair growth.

A patient who is hospitalized for an infection takes eplerenone [Inspra] for heart failure. Which medication, if ordered by the physician, should the nurse question? A.Ciprofloxacin [Cipro] B.Itraconazole [Sporanox] C.Tetracycline [Sumycin] D.Ampicillin [Principen]

•Answer: B •Rationale: Inhibitors of CYP3A4 can increase levels of eplerenone, thereby posing a risk of toxicity. Weak inhibitors (for example, erythromycin, saquinavir, verapamil, fluconazole) can double eplerenone levels. Strong inhibitors (for example, ketoconazole, itraconazole) can increase levels fivefold. If eplerenone is combined with a weak inhibitor, the eplerenone dosage should be reduced. Eplerenone should not be combined with a strong inhibitor.

A patient with type 2 diabetes mellitus is diagnosed with stable angina. Which beta blocker, if prescribed by the physician, would the nurse question? A. Metoprolol [Lopressor] B. Nadolol [Corgard] C. Bisoprolol [Zebeta] D. Atenolol [Tenormin]

•Answer: B •Rationale: Nonselective beta blockers such as nadolol [Corgard] should be avoided when treating patients with diabetes mellitus.

A patient is receiving a drug that blocks alpha1-adrenergic receptors. Which adverse effect, if experienced by the patient, is of most concern to the nurse? A. Nasal congestion B. Orthostatic hypotension C. Inhibition of ejaculation D. Reflex tachycardia

•Answer: B •Rationale: Orthostatic hypotension is the most serious adverse response to alpha-adrenergic blockade. This hypotension can reduce blood flow to the brain, thereby causing dizziness, lightheadedness, and even syncope (fainting).

The nurse instructs a patient about taking nifedipine [Procardia XL]. Which statement made by the patient indicates an understanding of medication teaching? A."I'll stop taking my beta blocker." B."The pill should be swallowed whole." C."The drug will cause constipation." D."This drug treats heart rhythm problems."

•Answer: B •Rationale: Patients should swallow sustained-release tablets whole, without crushing or chewing. Nifedipine may cause reflex tachycardia; beta blockers are prescribed to prevent reflex tachycardia. Nifedipine causes very little constipation. Nifedipine cannot be used to treat dysrhythmias.

A patient diagnosed with systemic lupus erythematosus (SLE) develops a dysrhythmia. Which medication, if ordered by the physician, should the nurse question? A.Lidocaine [Xylocaine] B.Procainamide [Procanbid] C.Disopyramide [Norpace] D.Amiodarone [Cordarone]

•Answer: B •Rationale: Procainamide is contraindicated in patients with systemic lupus erythematosus (SLE). SLE symptoms include pain and inflammation of the joints, pericarditis, fever, and hepatomegaly. Procainamide is associated with severe immunologic reactions; patients with SLE most likely will develop antinuclear antibodies (ANAs) directed against the patient's own nucleic acids, and SLE symptoms will worsen.

A patient plans to stop taking prescribed clonidine [Catapres] to treat hypertension because of the side effect of dry mouth. Which action by the nurse is best? A. Tell the patient that dry mouth is not caused by clonidine. B. Give the patient hard candy or gum to relieve the symptom. C. Instruct the patient to stop taking the medication immediately. D. Advise the patient to take a reduced dose of the medication.

•Answer: B •Rationale: Xerostomia (dry mouth) is common, occurring in about 40% of patients who are taking clonidine. The reaction usually diminishes over the first 2 to 4 weeks of therapy. Although not dangerous, xerostomia can be annoying enough to discourage drug use. Patients should be advised that discomfort can be reduced by chewing gum, sucking hard candy, and taking frequent sips of fluids.

A patient is prescribed a nitroglycerin transdermal patch. The nurse should include which statement when teaching the patient how to use this medication? A."Apply the patch to the chest over the heart." B."Change the patch each week." C."Remove the patch at bedtime." D."Put on the patch before exercising."

•Answer: C •Rationale: A transdermal nitroglycerin patch is applied once daily to a hairless area of skin. The site should be rotated to avoid local irritation. Tolerance develops if patches are used continuously. A patch-free interval of 10 to 12 hours is recommended. Patches are suited for sustained prophylaxis and will not abort an ongoing attack.

During administration of alteplase [Activase], the patient's IV site starts to ooze blood around the catheter. Which action by the nurse is most appropriate? A.Discontinue the infusion of alteplase. B.Assess the patient's vital signs. C.Apply direct pressure over the puncture site. D. Administer aminocaproic acid [Amicar].

•Answer: C •Rationale: Alteplase may cause bleeding, and the management of bleeding depends on its severity. Oozing at sites of cutaneous puncture can be controlled with direct pressure or a pressure dressing. If severe bleeding occurs, alteplase should be discontinued. Excessive fibrinolysis can be reversed with IV aminocaproic acid [Amicar], a compound that prevents activation of plasminogen and directly inhibits plasmin.

A patient has been diagnosed with a STEMI. Which medications does the nurse expect to be prescribed for this patient? A. Beta blocker, angiotensin II receptor blocker, and oxygen B. Aspirin, angiotensin-converting enzyme inhibitor, and diuretics C. Aspirin, beta blocker, oxygen, morphine, and nitroglycerin D. Heparin, nitroprusside, morphine, and calcium channel blocker

•Answer: C •Rationale: Aspirin, beta blocker, oxygen, morphine, and nitroglycerin are considered routine therapy for patients with ST-elevation myocardial infarction.

The nurse instructs a patient about doxazosin [Cardura]. Which statement by the patient to the nurse indicates an understanding of the instructions? A. "It is common to have nightmares and insomnia." B. "I need to take the medication on an empty stomach." C. "The medication should be taken tonight before I go to bed." D. "I should stop taking the medication if I feel lightheaded."

•Answer: C •Rationale: Doxazosin can cause orthostatic hypotension, reflex tachycardia, and nasal congestion. As with prazosin and terazosin, the first dose can cause profound hypotension, which can be minimized by giving the initial dose at bedtime.

A patient is prescribed digoxin [Lanoxin] and furosemide [Lasix]. It is most important for the nurse to assess which value before administering these medications? A.Serum sodium B.Blood urea nitrogen C.Serum potassium D.Plasma B-natriuretic peptide

•Answer: C •Rationale: Furosemide is a loop diuretic that promotes loss of potassium and thereby increases the risk of digoxin-induced dysrhythmias. When digoxin and furosemide are used concurrently, serum potassium levels must be monitored and maintained within a normal range (3.5 to 5 mEq/L).

The nurse teaches a patient diagnosed with chronic stable angina about the mechanism of action of nitroglycerin. The nurse should include which instruction? A."Nitroglycerin reduces vasospasms of the heart's arteries, which improves blood supply." B."Nitroglycerin opens the arteries to allow more oxygen to be delivered to the heart muscle." C."Nitroglycerin dilates veins, which decreases the amount of oxygen needed by the heart." D."Nitroglycerin improves blood flow to the heart muscle by increasing blood pressure."

•Answer: C •Rationale: Nitroglycerin relieves the pain of stable angina by dilating veins; this decreases venous return, which decreases preload, which decreases oxygen demand.

Which patient does the nurse identify as most likely needing an increased dose of warfarin [Coumadin] to have the same anticoagulant effect? A.Patient taking acetaminophen [Tylenol] for back pain B.Patient taking cimetidine [Tagamet] to prevent gastric ulcers C.Patient taking oral contraceptives to prevent pregnancy D.Patient taking prednisone [Deltasone] for rheumatoid arthritis

•Answer: C •Rationale: Oral contraceptives decrease the effects of warfarin; therefore, warfarin doses may need to be increased. Acetaminophen and cimetidine increase the effects of warfarin. Prednisone increases the risk of bleeding.

What is the antidote for heparin? A.Ferrous sulfate B.Atropine sulfate C.Protamine sulfate D.Magnesium sulfate

•Answer: C •Rationale: Protamine sulfate is an antidote to severe heparin overdose.

A patient is prescribed reserpine for hypertension. The nurse should monitor the patient for which adverse effect? A.Increased heart rate B.Elevated blood pressure C.Severe depression D.Decreased bowel sounds

•Answer: C •Rationale: Reserpine can produce severe depression that may persist for months after the drug is withdrawn. Suicide has occurred. The depletion of norepinephrine from sympathetic neurons can result in bradycardia, orthostatic hypotension, and nasal congestion. Via mechanisms that are not understood, reserpine can stimulate several aspects of gastrointestinal function. The drug can increase the secretion of gastric acid, which may result in ulcer formation. In addition, reserpine can increase the tone and motility of intestinal smooth muscle, thereby causing cramps and diarrhea.

A patient is prescribed spironolactone [Aldactone] for treatment of hypertension. Which foods should the nurse teach the patient to avoid? A.Baked fish B.Low-fat milk C.Salt substitutes D.Green beans

•Answer: C •Rationale: Spironolactone is a potassium-sparing diuretic. Medications that are potassium sparing, potassium supplements, and salt substitutes should be avoided. High-potassium foods should also be avoided.

A patient is prescribed verapamil [Calan]. The nurse should assess the patient for which common adverse effects? A.Atrial fibrillation, photosensitivity, and blurred vision B.Tachycardia, stomatitis, and inflammation of the joints C.Constipation, headache, and edema of the ankles and feet D.Dry mouth, lymphadenopathy, and decreased appetite

•Answer: C •Rationale: The adverse effects of verapamil occur secondary to vasodilation. Common adverse effects include constipation, dizziness, facial flushing, headache, and edema of the ankles and feet.

The nurse administers an intravenous infusion of amiodarone [Coredarone] to a patient to prevent recurrent episodes of ventricular fibrillation. It is most important for the nurse to assess the patient for which condition? A.Urinary retention B.Hypercalcemia C.Hypotension Metallic taste

•Answer: C •Rationale: The most common adverse effects of intravenous amiodarone are hypotension and bradydysrhythmias.

A patient has hypertension, type 2 diabetes, and chronic kidney disease. Which blood pressure goal would be most beneficial for this patient? A.Blood pressure less than 140/90 mm Hg B.Diastolic blood pressure less than 100 mm Hg C.Blood pressure less than 130/80 mm Hg D.Systolic blood pressure less than 160 mm Hg

•Answer: C •Rationale: The treatment goal for a person with hypertension and diabetes or chronic kidney disease is less than 130/80 mm Hg.

A patient who is taking spironolactone [Aldactone] is prescribed losartan [Cozaar]. The nurse should take which action? A.Assess for symptoms of hyperkalemia. B.Observe for a hypertensive crisis. C.Administer the medications as scheduled. D.Evaluate for first-dose hypotension.

•Answer: C •Rationale: These medications may be administered together without serious drug interactions. Spironolactone is a potassium-sparing diuretic, and losartan is an angiotensin II receptor blocker (ARB). The hypotensive effects of ARBs are additive with those of other antihypertensive drugs. When an ARB is added to an antihypertensive regimen, dosages of the other drugs may require reduction. The patient would be observed for hypotension (not first-dose hypotension).

The nurse is preparing to administer adenosine [Adenocard] to a patient to treat paroxysmal supraventricular tachycardia (SVT). Which action by the nurse is most appropriate? A.Inject the medication into the peripheral intravenous (IV) line. B.Infuse the dose by diluting the drug in 100 mL of saline. C.Administer a small test dose to determine hypersensitivity. D.Give the medication through the central line catheter.

•Answer: D •Rationale: Adenosine is intended for bolus IV administration; it is injected as close to the heart as possible and followed by a saline flush.

The nurse prepares to administer metoprolol [Lopressor] to a patient with chronic stable angina. What is a priority assessment to make before the administration of this medication? A. Temperature B. Urinary function C. Respiratory rate D. Heart rate

•Answer: D •Rationale: All beta blockers are contraindicated for patients with sinus bradycardia or AV heart block of more than the first degree, and they must be used with great caution in patients with heart failure. These are used with caution (especially the nonselective agents) in patients with asthma, bronchospasm, diabetes, or a history of severe allergic reactions. Use all beta blockers with caution in patients with a history of depression and in those taking calcium channel blockers.

A patient is to receive a scheduled dose of diltiazem [Cardizem]. The nurse should hold the medication and contact the prescriber if which of the following is noted? A.The patient's blood pressure is 112/64 mm Hg. B.The patient's cardiac rhythm is atrial fibrillation. C.The patient is complaining of chest pain. D.The patient is in second-degree heart block.

•Answer: D •Rationale: Diltiazem is contraindicated in patients with second-degree or third-degree heart block; diltiazem can exacerbate cardiac dysfunction.

A patient is receiving dopamine [Inotropin] for the treatment of shock. What would indicate to the nurse that the medication is effective? A.Decreased mean arterial pressure B.Gain of 2 kg in 24 hours C.Increased heart rate D.Increased urine output

•Answer: D •Rationale: Dopamine is used for the treatment of shock. Improved clinical status will best be monitored by assessing the patient's urine output. Dopamine will dilate renal blood vessels, improve renal perfusion, and increase urine output.

A female patient who is diabetic sustained an ST-elevation myocardial infarction (STEMI). The nurse provides discharge teaching. Which statement, made by the patient, indicates that further teaching is required? A."Medications are needed to prevent heart failure." B."I will take aspirin, atenolol, and captopril indefinitely." C."My blood pressure should be less than 130/80 mm Hg." D."Daily estrogen will prevent another heart attack."

•Answer: D •Rationale: Estrogen therapy for postmenopausal women is not effective as secondary prevention of another myocardial infarction and should not be initiated. In patients with acute MI, ACE inhibitors decrease severe heart failure. A post-MI patient should take a beta blocker, an ACE inhibitor, and an antiplatelet drug indefinitely. To prevent mortality after an MI, a diabetic patient's blood pressure should be less than 130/80 mm Hg.

A patient is prescribed sustained-release oral nitroglycerin capsules for chronic stable angina. The nurse should include which instruction? A."Avoid exercising to help prevent chest pain." B."Place the capsule under the tongue if chest pain occurs." C."Take the capsule as needed before exercise or exertion." D."Sit or lie down if dizziness or lightheadedness occurs."

•Answer: D •Rationale: Patients taking nitroglycerin should be instructed about symptoms of hypotension (for example, dizziness, lightheadedness) and advised to sit or lie down if these occur. Patients should be advised to avoid overexertion but should be encouraged to establish a regular program of aerobic exercise. Sustained-release nitroglycerin should be swallowed, not placed under the tongue. Sustained-release nitroglycerin is prescribed 1 to 4 times daily, not as needed.

Which patient would most likely be prescribed sodium nitroprusside [Nitropress]? A.A patient with a recent diagnosis of essential hypertension B.A patient with heart failure who receives weekly home visits C.A patient who is hypotensive after a myocardial infarction D.A patient with a hypertensive crisis in the intensive care unit

•Answer: D •Rationale: Sodium nitroprusside is used to treat hypertensive emergencies. The medication is administered intravenously, with continuous monitoring of blood pressure.

Which patient is the most appropriate candidate for both lifestyle changes and drug therapy with an antihypertensive medication? A.A 47-year-old patient with blood pressure of 110/78 mm Hg and with type 2 diabetes mellitus B.A 76-year-old patient with blood pressure of 128/88 mm Hg and a history of dyslipidemia C.A 52-year-old patient with blood pressure of 136/89 mm Hg who smokes 1 pack of cigarettes per day D.A 32-year-old patient with blood pressure of 142/94 mm Hg who is sedentary

•Answer: D •Rationale: Stages 1 and 2 hypertension should be treated with both lifestyle changes and drug therapy to control blood pressure.

A patient in the emergency department is diagnosed with ST-elevation myocardial infarction (STEMI). The patient has been prescribed 325 mg of aspirin. Which action by the nurse is appropriate? A. Administer the medication to the patient if a headache develops. B. Administer the medication with a full glass of water. C. Instruct the patient to let the tablet dissolve under the tongue. D. Tell the patient to chew the tablet thoroughly.

•Answer: D •Rationale: The first dose of aspirin should be given immediately. The dose (162-325 mg) is chewed to allow rapid absorption across the buccal mucosa. Aspirin suppresses platelet aggregation and thereby decreases mortality, reinfarction, and stroke. All patients should chew a 162- to 325-mg dose upon hospital admission and should take 81 to 162 mg/day indefinitely after discharge.

The nurse cares for a patient who is prescribed oral bumetanide twice daily. It is most important for the nurse to take which action? A. Monitor the patient for signs and symptoms of hyperkalemia. B. Insert a urinary catheter and assess the hourly urine output. C. Weigh the patient before administering each dose. D. Schedule the medication to be given at 0800 and 1400.

•Answer: D •Rationale: The nurse should administer oral bumetanide with twice-a-day dosing at 0800 and 1400 to minimize nocturia. Daily weights should be obtained in the morning before eating. Patients receiving IV bumetanide are more likely to need hourly monitoring of urine output with a urinary catheter. Bumetanide may cause hypokalemia; signs and symptoms of hypokalemia include irregular heartbeat, muscle weakness, cramping, flaccid paralysis, leg discomfort, extreme thirst, and confusion.

Mannitol IV has been ordered for the patient. When the IV solution of mannitol arrives from the pharmacy, the nurse notes crystals in the fluid. What is the most appropriate action by the nurse?

•Mannitol may crystallize out of solution if exposed to a low temperature. Accordingly, preparations should be observed for crystals before use. Preparations that contain crystals should be warmed (to redissolve the mannitol) and then cooled to body temperature for administration.

A patient who sustained a head injury is admitted to the critical care unit with increased intracranial pressure (ICP). The healthcare provider says that a diuretic will be used to lower the patient's ICP. The nurse anticipates that which diuretic will be ordered, and why?

•The nurse anticipates that mannitol, an osmotic diuretic, will be ordered. Intracranial pressure (ICP) that has been elevated by cerebral edema can be reduced with mannitol. The drug lowers ICP because its presence in the blood vessels of the brain creates an osmotic force that draws edematous fluid from the brain into the blood. There is no risk of increasing cerebral edema because mannitol cannot exit the capillary beds of the brain.