Pharmacology II Final Exam

A nurse is caring for a client who will begin using transdermal nitroglycerin to treat angina pectoris. When speaking to the client about the drug, which of the following instructions should the nurse include?

"apply the patch to a hairless area and rotate sites" "apply a new patch when you start your day" "remove patches for 10 to 12 hours each day"

ACE inhibitors adverse effects

"prils make you ill" ACE inhibitors are generally well tolerated. Some adverse effects (e.g., first-dose hypotension, hyperkalemia) are due to a reduction in angiotensin II, whereas others (cough, angioedema) are due to elevation of bradykinin. -First-Dose Hypotension, cough, hyperkalemia, renal failure, angioedema, neutropenia -Fetal Injury: use of ACE inhibitors during the second and third trimesters of pregnancy can injure the developing fetus. Specific effects include hypotension, hyperkalemia, skull hypoplasia, pulmonary hypoplasia, anuria, renal failure (reversible and irreversible), and death.

Treating hypertension of special populations

-African Americans. Hypertension is a major health problem for African American adults. Hypertension develops earlier, has a much higher incidence, and is likely to be more severe. As a result, African Americans face a greater risk of heart disease, end-stage renal disease, and stroke. -hypertension often goes untreated in African Americans and can already have severe organ failure when addressed -Children and Adolescents. The incidence of secondary hypertension in children is much higher than in adults. Accordingly, efforts to diagnose and treat an underlying cause should be especially diligent. For children with primary hypertension, treatment is the same as for adults—although doses are lower and should be adjusted with care. Because ACE inhibitors and ARBs can cause fetal harm, they should be avoided in girls who are sexually active or pregnant. -Older adults By age 65 years, most Americans have hypertension. Furthermore, high BP in this group almost always presents as isolated systolic hypertension; DBP is usually normal or low. The good news, as shown in the Hypertension in the Very Elderly Trial (HYVET), is that treatment can reduce the incidence of heart failure, fatal stroke, and all-cause mortality. Most older people are not treated.

ACE inhibitors drug interactions

-Diuretics. Diuretics may intensify first-dose hypotension. To prevent this interaction, diuretics should be withdrawn 2 to 3 days before giving an ACE inhibitor. Diuretic therapy can be resumed later if needed. -Antihypertensive Agents. The hypotensive effects of ACE inhibitors are often additive with those of other antihypertensive drugs (e.g., diuretics, sympatholytics, vasodilators, calcium channel blockers). When an ACE inhibitor is added to an antihypertensive regimen, dosages of other drugs may require reduction. -Drugs That Raise Potassium Levels. ACE inhibitors increase the risk of hyperkalemia caused by potassium supplements and potassium-sparing diuretics. The risk of hyperkalemia is increased because, by suppressing aldosterone secretion, ACE inhibitors can reduce excretion of potassium. To minimize the risk of hyperkalemia, potassium supplements and potassium-sparing diuretics should be employed only when clearly indicated. -Lithium. ACE inhibitors can cause lithium to accumulate to toxic levels. Lithium levels should be monitored frequently. -Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). Aspirin, ibuprofen, and other NSAIDs may reduce the antihypertensive effects of ACE inhibitors.

Ongoing Evaluation and Interventions CCB

-Evaluating Therapeutic Effects -Minimizing Adverse Effects *Reflex Tachycardia. --Reflex tachycardia can be suppressed with a beta blocker. *Peripheral Edema. --Inform patients about signs of edema and instruct them to notify the prescriber if these occur. If necessary, edema can be reduced with a diuretic. -Managing Acute Toxicity

Sodium Nitroprusside adverse effects

-Excessive Hypotension: If administered too rapidly, nitroprusside can cause a precipitous drop in blood pressure, resulting in headache, palpitations, nausea, vomiting, and sweating. Blood pressure should be monitored continuously. -Cyanide Poisoning: Rarely, lethal amounts of cyanide have accumulated. Cyanide buildup is most likely in patients with liver disease and in those with low stores of thiosulfate, the cofactor needed for cyanide detoxification. The chances of cyanide poisoning can be minimized by avoiding rapid infusion (faster than 5 mcg/kg/min) and by coadministering thiosulfate. If cyanide toxicity occurs, nitroprusside should be withdrawn. -Thiocyanate Toxicity: When nitroprusside is given for several days, thiocyanate may accumulate. Although much less hazardous than cyanide, thiocyanate can also cause adverse effects. These effects, which involve the central nervous system, include disorientation, psychotic behavior, and delirium. To minimize toxicity, patients receiving nitroprusside for more than 3 days should undergo monitoring of plasma thiocyanate, which must be kept below 0.1 mg/mL.

Drugs to avoid for pts in stage C HF

-Patients in Stage C should avoid three classes of drugs: antidysrhythmics, calcium channel blockers (CCBs), and NSAIDs (e.g., aspirin) • Antidysrhythmic agents—These drugs have cardiosuppressant and prodysrhythmic actions that can make HF worse. Only two agents—amiodarone [Cordarone] and dofetilide [Tikosyn]—have been proven not to reduce survival. • Calcium channel blockers—These drugs can make HF worse and may increase the risk of adverse cardiovascular events. Only the long-acting dihydropyridine CCBs, such as amlodipine [Norvasc], have been shown not to reduce survival. • NSAIDs—These drugs promote sodium retention and peripheral vasoconstriction. Both actions can make HF worse. In addition, NSAIDs can reduce the efficacy and intensify the toxicity of diuretics and ACE inhibitors. Hence, even though aspirin has beneficial effects on coagulation, it should still be avoided unless clinically indicated for conditions such as myocardial infarction.

Hydralazine adverse effects

-Reflex Tachycardia: By lowering arterial blood pressure, hydralazine can trigger reflex stimulation of the heart, thereby causing cardiac work and myocardial oxygen demand to increase. Because hydralazine-induced reflex tachycardia is frequently severe, the drug is usually combined with a beta blocker. -Increased Blood Volume: Hydralazine-induced hypotension can cause sodium and water retention and a corresponding increase in blood volume. A diuretic can prevent volume expansion. -Systemic Lupus Erythematosus-like Syndrome: Hydralazine can cause an acute rheumatoid syndrome that closely resembles systemic lupus erythematosus (SLE). Symptoms include muscle pain, joint pain, fever, nephritis, pericarditis, and the presence of antinuclear antibodies. The syndrome occurs most frequently in slow acetylators and is rare when dosage is kept below 200 mg/day. If an SLE-like reaction occurs, hydralazine should be discontinued. Symptoms are usually reversible but may take 6 or more months to resolve. In some cases, rheumatoid symptoms persist for years. -Other Adverse Effects: Common responses include headache, dizziness, weakness, and fatigue. These reactions are related to hydralazine-induced hypotension.

Gemfibrozil nursing implications

-Therapeutic Goal: Gemfibrozil, in conjunction with diet modification, is used to reduce elevated levels of TGs (VLDLs). The drug is not very effective at lowering LDL cholesterol. It may also be used to raise low levels of HDL cholesterol. -Baseline Data: Obtain laboratory values for total cholesterol, LDL cholesterol, HDL cholesterol, and TGs (VLDLs). -Identifying High-Risk Patients: ***Gemfibrozil is contraindicated for patients with liver disease, severe renal dysfunction, and gallbladder disease. **Use with caution in patients taking statins or warfarin. Implementation: Administration -Route: Oral. -Administration: Instruct patients to administer gemfibrozil 30 minutes before the morning and evening meals. Ongoing Evaluation and Interventions -Evaluating Therapeutic Effects: Obtain periodic tests of blood lipids. -Minimizing Adverse Effects: Gallstones. Gemfibrozil increases gallstone development. Inform patients about symptoms of gallbladder disease (e.g., upper abdominal discomfort, intolerance of fried foods, bloating), and instruct them to notify the prescriber if these develop. Myopathy. Gemfibrozil can cause muscle damage. Warn patients to report any signs of muscle injury, such as tenderness, weakness, or unusual muscle pain. Liver Disease. Gemfibrozil may disrupt liver function. Cancer of the liver may also be a risk. Obtain periodic tests of liver function.

Direct Renin Inhibitor MOA

-aliskiren Aliskiren binds tightly with renin and thereby inhibits the cleavage of angiotensinogen into angiotensin I. Since this reaction is the first and rate-limiting step in the production of angiotensin II and aldosterone, aliskiren can reduce the influence of the entire RAAS.

Aldosterone Antagonists MOA

-eplerenone, selective aldosterone receptor blocker Eplerenone produces selective blockade of aldosterone receptors, having little or no effect on receptors for other steroid hormones (e.g., glucocorticoids, progesterone, androgens). In the kidney, activation of aldosterone receptors promotes excretion of potassium and retention of sodium and water. Receptor blockade has the opposite effect: retention of potassium and increased excretion of sodium and water. Loss of sodium and water reduces blood volume, and hence blood pressure. Blockade of aldosterone receptors at nonrenal sites may prevent or reverse pathologic effects of aldosterone on cardiovascular structure and function.

ARBs therapeutic uses

-hypertension: All ARBs are approved for hypertension. Reductions in blood pressure equal those seen with ACE inhibitors. -heart failure: only two ARBs—valsartan [Diovan] and candesartan [Atacand]—are approved for heart failure -Diabetic Nephropathy: Two ARBs—irbesartan [Avapro] and losartan [Cozaar]—are approved for managing nephropathy in hypertensive patients with type 2 diabetes -Myocardial Infarction: One ARB—valsartan [Diovan]—is approved for reducing cardiovascular mortality in post-MI patients with heart failure or LV dysfunction -Stroke Prevention: One ARB—losartan [Cozaar]—is approved for reducing the risk of stroke in patients with hypertension and LV hypertrophy. -Prevention of MI, Stroke, and Death in Patients at High Cardiovascular Risk: One ARB—telmisartan [Micardis]—is approved for reducing the risk of MI, stroke, and death from cardiovascular causes in patients age 55 years and older, but only if they are intolerant of ACE inhibitors -Diabetic Retinopathy: losartan

When are ACE inhibitors contraindicated?

ACE inhibitors are contraindicated for patients with bilateral renal artery stenosis (or stenosis in the artery to a single remaining kidney), can cause renal failure

ACE inhibitors safety alert

ACE inhibitors can cause angioedema, a potentially life-threatening reaction. If patients report edema of the tongue, lips, or eyes, emergency care should be sought immediately, and the patient must never take ACE inhibitors again.

Angiotensin-Converting Enzyme Inhibitors MOA

ACE inhibitors produce their beneficial effects and adverse effects by (1) reducing levels of angiotensin II (through inhibition of ACE) and (2) increasing levels of bradykinin (through inhibition of kinase II). By reducing levels of angiotensin II, ACE inhibitors can dilate blood vessels (primarily arterioles and to a lesser extent veins), reduce blood volume (through effects on the kidney), and, importantly, prevent or reverse pathologic changes in the heart and blood vessels mediated by angiotensin II and aldosterone. -Suffix: pril -Captopril is prototype

Angiotensin II Receptor Blockers MOA

ARBs block access of angiotensin II to its receptors in blood vessels, the adrenals, and all other tissues. As a result, ARBs have effects much like those of the ACE inhibitors. In contrast to the ACE inhibitors, ARBs do not inhibit kinase II, and hence do not increase levels of bradykinin in the lung. As a result, ARBs have a lower risk of cough, the most common reason for stopping ACE inhibitors. -suffix: sartan -Prototype: losartan

Hydralazine pharmacokinetics

Absorption and Time Course of Action: Hydralazine is readily absorbed following oral administration. Effects begin within 45 minutes and persist for 6 hours or longer. With parenteral administration, effects begin faster (within 10 minutes) and last 2 to 4 hours. Metabolism: Hydralazine is inactivated by a metabolic process known as acetylation. The ability to acetylate drugs is genetically determined. Some people are rapid acetylators; some are slow acetylators. The distinction between rapid and slow acetylators can be clinically significant because individuals who acetylate hydralazine slowly are likely to have higher blood levels of the drug, which can result in excessive vasodilation and other undesired effects. To avoid hydralazine accumulation, dosage should be reduced in slow acetylators.

Digoxin absorption

Absorption with digoxin tablets is variable, ranging between 60% and 80%, and can be decreased by certain foods and drugs. Meals high in bran can decrease absorption significantly, as can cholestyramine, kaolin-pectin, and certain other drugs (see Table 48.2). Of note, taking digoxin with meals decreases the rate of absorption but not the extent. In the past, there was considerable variability in the absorption of digoxin from tablets prepared by different manufacturers. This variability resulted from differences in the rate and extent of tablet dissolution. Because of this variable bioavailability, it had been recommended that patients not switch between different digoxin brands. Today, bioavailability of digoxin in tablets produced by different companies is fairly uniform, making brands of digoxin more interchangeable than in the past. However, given the narrow therapeutic range of digoxin, some authorities still recommend that patients not switch between brands of digoxin tablets—even when prescriptions are written generically—except with the approval and supervision of the prescriber.

Nitroglycerin pharmacokinetics

Absorption. Nitroglycerin is highly lipid soluble and crosses membranes with ease. Because of this property, nitroglycerin can be administered by uncommon routes (sublingual, buccal, transdermal), as well as by more conventional routes (oral, intravenous). Metabolism. Nitroglycerin undergoes rapid inactivation by hepatic enzymes (organic nitrate reductases). As a result, the drug has a plasma half-life of only 5 to 7 minutes. When nitroglycerin is administered orally, most of each dose is destroyed on its first pass through the liver.

Diltiazem adverse effects

Adverse effects are like those of verapamil, except that diltiazem causes less constipation. The most common effects are dizziness, flushing, headache, and edema of the ankles and feet. Like verapamil, diltiazem can exacerbate cardiac dysfunction in patients with bradycardia, sick sinus syndrome, heart failure, or second-degree or third-degree AV block. Like other CCBs, diltiazem may cause chronic eczematous rash in older adults.

verapamil therapeutic uses

Angina Pectoris. -Verapamil is used widely to treat angina pectoris. The drug is approved for vasospastic angina and angina of effort. Benefits in both disorders derive from vasodilation. Essential Hypertension. -Verapamil is a second-line agent for chronic hypertension, used after thiazide diuretics. The drug lowers blood pressure by dilating arterioles. Cardiac Dysrhythmias. -Verapamil, administered IV, is used to slow ventricular rate in patients with atrial flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia. Benefits derive from suppressing impulse conduction through the AV node, thereby preventing the atria from driving the ventricles at an excessive rate.

Digoxin Special Interest Topic

Attention: Digoxin May Be Hazardous to Women's Health for women with heart failure digoxin may do more harm than good. the drug should be reserved for patients who have not responded adequately to first-line medicines: ACE inhibitors or ARBs, diuretics, and beta blockers. Furthermore, digoxin levels should be kept as low as possible (0.5 to 0.8 ng/mL is a reasonable initial target).

HF Stage A

By definition, patients in ACC/AHA Stage A have no symptoms of HF and no structural or functional cardiac abnormalities—but they do have behaviors or conditions strongly associated with developing HF. Important among these are hypertension, coronary artery disease, diabetes, family history of cardiomyopathy, and a personal history of alcohol abuse, rheumatic fever, or treatment with a cardiotoxic drug (e.g., doxorubicin, trastuzumab). Management is directed at reducing risk. Hypertension, hyperlipidemia, and diabetes should be controlled, as should ventricular rate in patients with supraventricular tachycardias. An ACE inhibitor or ARB can be useful for patients with diabetes, atherosclerosis, or hypertension. Patients should cease behaviors that increase HF risk, especially smoking and alcohol abuse. (Excessive, chronic consumption of alcohol is a leading cause of cardiomyopathy. In patients with HF, acute alcohol consumption can suppress contractility.) There is no evidence that getting regular exercise can prevent development of HF, although exercise does have other health benefits. Routine use of dietary supplements to prevent structural heart disease is not recommended.

Digoxin adverse effects I

Cardiac Dysrhythmias Dysrhythmias are the most serious adverse effect of digoxin. They result from altering the electrical properties of the heart. Fortunately, when used in the dosages recommended today, dysrhythmias are uncommon. -can result from: • Decreased automaticity of the SA node • Decreased impulse conduction through the AV node • Spontaneous discharge of Purkinje fibers (caused in part by increased automaticity) • Shortening of the effective refractory period in ventricular muscle

clinical manifestations and treatment of verapamil toxicity

Clinical Manifestations: --Overdose can produce severe hypotension and cardiotoxicity (bradycardia, AV block). Treatment: -General Measures. Verapamil can be removed from the GI tract with gastric lavage followed by activated charcoal. Intravenous calcium gluconate can counteract both vasodilation and negative inotropic effects, but will not reverse AV block. -Hypotension. Hypotension can be treated with IV norepinephrine, which promotes vasoconstriction (by activating alpha1 receptors on blood vessels) and increases cardiac output (by activating beta1 receptors in the heart). Placing the patient in modified Trendelenburg's position (legs elevated) and administering IV fluids may also help. -Bradycardia and AV Block. Bradycardia and AV block can be treated with atropine (an anticholinergic drug that blocks parasympathetic influences on the heart). If pharmacologic measures are inadequate, electronic pacing may be required. Use of glucagon in animal models has improved heart rate through increasing amounts of intracellular cyclic AMP. It has been used successfully in treating human cases of CCB toxicity.

verapamil adverse effects

Common Effects. Verapamil is generally well tolerated. Constipation occurs frequently and is the most common complaint. This problem, which can be especially severe in older adults, can be minimized by increasing dietary fluids and fiber. Constipation results from blockade of calcium channels in smooth muscle of the intestine. Other common effects—dizziness, facial flushing, headache, and edema of the ankles and feet—occur secondary to vasodilation. Cardiac Effects. Blockade of calcium channels in the heart can compromise cardiac function. In the SA node, calcium channel blockade can cause bradycardia; in the AV node, blockade can cause partial or complete AV block; and in the myocardium, blockade can decrease contractility. When the heart is healthy, these effects rarely have clinical significance. However, in patients with certain cardiac diseases, verapamil can seriously exacerbate dysfunction. Accordingly, the drug must be used with special caution in patients with cardiac failure, and it must not be used at all in patients with sick sinus syndrome or second-degree or third-degree AV block. Other Effects. In older patients, CCBs have been associated with chronic eczematous eruptions, typically starting 3 to 6 months after treatment onset. If the reaction is mild, switching to a different CCB may help. If the condition is severe, use of verapamil and other CCBs should stop. -Gingival hyperplasia (overgrowth of gum tissue) has been reported.

Inotropic Agents- digoxin

Digoxin belongs to a class of drugs known as cardiac glycosides, agents best known for their positive inotropic actions, that is, their ability to increase myocardial contractile force. By increasing contractile force, digoxin can increase cardiac output. In addition, it can alter the electrical activity of the heart, and it can favorably affect neurohormonal systems. Unfortunately, although digoxin can reduce symptoms of HF, it does not prolong life. Used widely in the past, digoxin is considered a second-line agent today. The pharmacology of digoxin is discussed later.

Digoxin distribution

Digoxin is distributed widely and crosses the placenta. High levels are achieved in cardiac and skeletal muscle, owing largely to binding to Na+/K+-ATPase. About 23% of digoxin in plasma is bound to proteins, mainly albumin.

Digoxin elimination

Digoxin is eliminated primarily by renal excretion. Hepatic metabolism is minimal. Because digoxin is eliminated by the kidneys, renal impairment can lead to toxic accumulation. Accordingly, dosage must be reduced if kidney function declines. Because digoxin is not metabolized to a significant extent, changes in liver function do not affect digoxin levels.

A nurse is caring for a client who is about to begin captopril therapy. Which of the following adverse effects should the nurse instruct the client to report because it can indicate a need to discontinue drug therapy?

Distorted taste Swelling of the tongue rash dry cough

Digoxin drug interactions

Diuretics Thiazide diuretics and loop diuretics promote loss of potassium and thereby increase the risk of digoxin-induced dysrhythmias. Accordingly, when digoxin and these diuretics are used concurrently, serum potassium levels must be monitored and maintained within the normal range (3.5 to 5 mEq/L). If hypokalemia develops, potassium levels can be restored with potassium supplements, a potassium-sparing diuretic, or both. ACE Inhibitors and ARBs These drugs can increase potassium levels and can thereby decrease therapeutic responses to digoxin. Exercise caution if an ACE inhibitor or ARB is combined with potassium supplements or a potassium-sparing diuretic. Sympathomimetics Sympathomimetic drugs (e.g., dopamine, dobutamine) act on the heart to increase the rate and force of contraction. The increase in contractile force can add to the positive inotropic effects of digoxin. These complementary actions can be beneficial. In contrast, the ability of sympathomimetics to increase heart rate may be detrimental in that the risk of a tachydysrhythmia is increased. Quinidine Quinidine is an antidysrhythmic drug that can cause plasma levels of digoxin to rise. Quinidine increases digoxin levels by (1) displacing digoxin from tissue binding sites and (2) reducing renal excretion of digoxin. By elevating levels of free digoxin, quinidine can promote digoxin toxicity. Accordingly, concurrent use of quinidine and digoxin should be avoided. Verapamil Verapamil, a calcium channel blocker, can significantly increase plasma levels of digoxin. If the combination is employed, digoxin dosage must be reduced. In addition, verapamil can suppress myocardial contractility and can thereby counteract the benefits of digoxin.

Drug therapy for atherosclerotic CV disease

Drugs are not the first-line therapy for lowering LDL cholesterol. Rather, drugs should be employed only if TLCs fail to reduce LDL cholesterol to an acceptable level—and then only if the combination of elevated LDL cholesterol and the patient's ASCVD risk category justify drug use. When drugs are used, it is essential that lifestyle modification continues because the beneficial effects of diet and drugs are additive; drugs alone may be unable to achieve the LDL goal. It is important to note that the principal benefit of drug therapy is primary prevention: Drugs are much better at preventing or slowing ASCVD than at promoting regression of established coronary atherosclerosis. Furthermore, because LDL cholesterol levels will return to pretreatment values if drugs are withdrawn, treatment must continue lifelong. Patients should be made aware of this requirement.

Ezetimibe MOA

Ezetimibe acts on cells of the brush border of the small intestine to inhibit dietary cholesterol absorption. The drug also inhibits reabsorption of cholesterol secreted in the bile. Treatment reduces plasma levels of total cholesterol, LDL cholesterol, TGs, and apolipoprotein B. In addition, ezetimibe can produce a small increase in HDL cholesterol.

vasodilators safety alert

Falls: Vasodilators place patients at increased risk of falls. Patients receiving vasodilators should be informed about symptoms of hypotension (light-headedness, dizziness) and advised to sit or lie down if these occur. Failure to follow this advice may result in fainting. Patients should also be taught that they can minimize hypotension by avoiding abrupt transitions from a supine or seated position to an upright position.

Gemfibrozil therapeutic use

Gemfibrozil is used primarily to reduce high levels of plasma triglycerides (VLDLs). Treatment is limited to patients who have not responded adequately to weight control and diet modification. Gemfibrozil can also reduce LDL cholesterol slightly. However, other drugs (statins, cholestyramine, colestipol) are much more effective. Gemfibrozil can be used to raise HDL cholesterol, although it is not approved for this application. When tested in patients with normal LDL cholesterol and low HDL cholesterol, gemfibrozil reduced the risk of major CV events—but did not reduce mortality from ASCVD. Because LDL cholesterol was normal, it appears that benefits were due primarily to elevation of HDL cholesterol, along with reduction of plasma TGs.

Carvedilol therapeutic uses

HF, HTN

A nurse is caring for a client who has a new prescription for aliskiren to treat hypertension. the nurse should monitor the client for which of the following findings as an adverse effect of the drug?

Hyperkalemia throat swelling cough

Treatment of unstable angina

IV access, pain control, oxygen Anti-ischemic therapy consists of: • Nitroglycerin—give three doses sublingually every 5 minutes (tablet or spray) and follow with IV therapy in the event of persistent ischemia or hypertension. • A beta blocker—give the first dose IV if chest pain is ongoing. If beta blockers are contraindicated, substitute a nondihydropyridine calcium channel blocker (verapamil or diltiazem). • Supplemental oxygen—for patients with cyanosis or respiratory distress. • Intravenous morphine sulfate—if pain is not relieved immediately by nitroglycerin, or if pulmonary congestion or severe agitation is present. • An angiotensin-converting enzyme inhibitor—for patients with left ventricular dysfunction or congestive heart failure. Angiotensin receptor blockers are a reasonable alternative in patients who have intolerance to angiotensin-converting enzyme inhibitors. Antiplatelet therapy, which should be started promptly, consists of: • Aspirin—continue indefinitely. • Clopidogrel [Plavix], prasugrel [Effient], or ticagrelor [Brilinta]—continue for up to 2 months. • Abciximab [ReoPro], a glycoprotein IIb/IIIa inhibitor—but only if angioplasty is planned. • Eptifibatide [Integrilin] or tirofiban [Aggrastat] (both are glycoprotein IIb/IIIa inhibitors)—but only in high-risk patients with continuing ischemia, and only if angioplasty is not planned. Anticoagulant therapy consists of subcutaneous low-molecular-weight heparin (e.g., enoxaparin [Lovenox]), direct thrombin inhibitors (bivalirudin [Angiomax]), factor Xa inhibitors (fondaparinux [Arixtra]), or IV unfractionated heparin.

Doxazosin therapeutic uses

Immediate-release forms of this drug are indicated for hypertension and BPH. Extended-release doxazosin [Cardura XL] is approved for management of BPH only.

Nifedipine safety alert

Immediate-release nifedipine has been associated with increased mortality in patients with myocardial infarction and unstable angina. Other IR CCBs have been associated with an increased risk of myocardial infarction in patients with hypertension. However, in both cases, a causal relationship has not been established. Nonetheless, the National Heart, Lung, and Blood Institute has recommended that immediate-release nifedipine, especially in higher doses, be used with great caution, if at all. It is important to note that these adverse effects have not been associated with sustained-release nifedipine or with any other long-acting CCB.

Inotropic Agents (Other Than Digoxin)

In addition to digoxin, we have two other types of inotropic drugs: sympathomimetics and phosphodiesterase (PDE) inhibitors. Unlike digoxin, which can be taken orally, these other inotropics must be given by IV infusion. Accordingly, their use is restricted to acute care of hospitalized patients. Because digoxin can be given PO, it is the only inotropic agent suited for long-term therapy. -Sympathomimetic Drugs: Dopamine and Dobutamine. -Phosphodiesterase Inhibitors: Milrinone

Sodium Nitroprusside CV effects

In contrast to hydralazine and minoxidil, nitroprusside causes venous dilation in addition to arteriolar dilation. Curiously, although nitroprusside is an effective arteriolar dilator, reflex tachycardia is minimal. Administration is by IV infusion, and effects begin at once. By adjusting the infusion rate, blood pressure can be decreased to almost any level desired. When the infusion is stopped, blood pressure returns to pretreatment levels in minutes. Nitroprusside can trigger retention of sodium and water; furosemide can help counteract this effect.

Vasodilators (Other Than ACE Inhibitors and ARBs)

Isosorbide Dinitrate Plus Hydralazine -For treatment of HF, isosorbide dinitrate (ISDN) and hydralazine are usually combined. The combination represents an alternative to ACE inhibitors or ARBs. However, ACE inhibitors and ARBs are generally preferred.

HF Stage B

Like patients in Stage A, those in Stage B have no signs or symptoms of HF, but they do have structural heart disease that is strongly associated with the development of HF. Among these structural changes are LV hypertrophy or fibrosis, LV dilation or hypocontractility, valvular heart disease, and previous myocardial infarction. The goal of management is to prevent development of symptomatic HF. The approach is to implement measures that can prevent further cardiac injury, delaying the progression of remodeling and LV dysfunction. Specific measures include all those discussed for Stage A. In addition, treatment with an ACE inhibitor plus a beta blocker is recommended for all patients with a reduced ejection fraction, history of myocardial infarction, or both. For patients who cannot tolerate ACE inhibitors, an ARB may be used instead. As in Stage A, there is no evidence that using dietary supplements or getting regular exercise can help prevent progression to symptomatic HF.

metroprolol Precautions, Warnings, and Contraindications

Like propranolol, metoprolol is contraindicated for patients with sinus bradycardia and AV block greater than first degree. In addition, it should be used with great care in patients with heart failure. Because metoprolol produces only minimal blockade of beta2 receptors, the drug is safer than propranolol for patients with asthma or a history of severe allergic reactions. In addition, because metoprolol does not suppress beta2-mediated glycogenolysis, it can be used more safely than propranolol by patients with diabetes. Please note, however, that metoprolol, like propranolol, will mask common signs and symptoms of hypoglycemia, thereby depriving the diabetic patient of an early indication that hypoglycemia is developing.

Diltiazem actions and uses

Like verapamil, diltiazem [Cardizem, Dilacor XR, Tiazac, others] blocks calcium channels in the heart and blood vessels. As a result, the actions and applications of verapamil and diltiazem are very similar. Diltiazem has the same effects on cardiovascular function as verapamil. Both drugs lower blood pressure through arteriolar dilation, and because their direct suppressant actions are balanced by reflex cardiac stimulation, both have little net effect on the heart. Like verapamil, diltiazem is used for angina pectoris, essential hypertension, and cardiac dysrhythmias (atrial flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia).

Diltiazem drug and food interactions

Like verapamil, diltiazem can exacerbate digoxin-induced suppression of AV conduction and can intensify the cardiosuppressant effects of beta blockers. Patients receiving diltiazem concurrently with digoxin or a beta blocker should be monitored closely for cardiac status. As with verapamil, grapefruit juice can significantly increase levels of diltiazem.

A nurse is caring for a client who has a new prescription for dobutamine. The nurse should clarify the prescription with the provider if the client is receiving which of the following types of drugs?

MAOI General anesthetic Tricyclic antidepressant Beta blocker

Metroprolol Adverse Effects

Major adverse effects involve the heart. Like propranolol, metoprolol can cause bradycardia, reduced cardiac output, AV heart block, and rebound cardiac excitation following abrupt withdrawal. Also, even though metoprolol is approved for treating heart failure, it can cause heart failure if used incautiously. In contrast to propranolol, metoprolol causes minimal bronchoconstriction and does not interfere with beta2-mediated glycogenolysis.

Digoxin adverse effects III

Measures to Reduce Adverse Effects -Patient education can help reduce the incidence of toxicity. Patients should be warned about digoxin-induced dysrhythmias and instructed to take their medication exactly as prescribed. In addition, they should be informed about symptoms of developing toxicity (altered heart rate or rhythm, visual or GI disturbances) and instructed to notify the prescriber if these develop. If a potassium supplement or potassium-sparing diuretic is part of the regimen, it should be taken exactly as ordered.

Metroprolol Pharmacokinetics

Metoprolol is very lipid soluble and well absorbed following oral administration. Like propranolol, metoprolol undergoes extensive metabolism on its first pass through the liver. As a result, only 40% of an oral dose reaches the systemic circulation. Elimination is by hepatic metabolism and renal excretion.

A nurse is teaching a client who has a new prescription for quinidine. Which of the following statements should the nurse include?

Monitor your pulse rate and report changes

A nurse is caring for a client who is taking atorvastatin and has a new prescription for gemfibrozil. The nurse should recognize that this drug combination places the client at an increased risk for which of the following adverse effects?

Myopathy

Nitroglycerin adverse effects

Nitroglycerin is generally well tolerated. Principal adverse effects—headache, hypotension, and tachycardia—occur secondary to vasodilation. Headache. Initial therapy can produce severe headache. This response diminishes over the first few weeks of treatment. In the meantime, headache can be reduced with aspirin, acetaminophen, or some other mild analgesic. Orthostatic Hypotension. Relaxation of VSM causes blood to pool in veins when the patient assumes an erect posture. Pooling decreases venous return to the heart, which reduces cardiac output, causing blood pressure to fall. Symptoms of orthostatic hypotension include light-headedness and dizziness. Patients should be instructed to sit or lie down if these occur. Lying with the feet elevated promotes venous return and can help restore blood pressure. Reflex Tachycardia. Nitroglycerin lowers blood pressure—primarily by decreasing venous return and partly by dilating arterioles. By lowering blood pressure, the drug can activate the baroreceptor reflex, causing sympathetic stimulation of the heart. The resultant increase in both heart rate and contractile force increases cardiac oxygen demand, which negates the benefits of therapy. Pretreatment with a beta blocker or verapamil (a calcium channel blocker that directly suppresses the heart) can prevent sympathetic cardiac stimulation.

Sodium Nitroprusside therapeutic use- hypertensive emergency

Nitroprusside is used to lower blood pressure rapidly in hypertensive emergencies. Oral antihypertensive medication should be initiated simultaneously. During nitroprusside treatment, furosemide may be needed to prevent excessive retention of fluid.

Digoxin adverse effects II

Noncardiac Adverse Effects Anorexia, nausea, and vomiting are the most common GI side effects. These responses result primarily from stimulation of the chemoreceptor trigger zone of the medulla. Digoxin rarely causes diarrhea. Fatigue is the most frequent CNS effect. Visual disturbances (e.g., blurred vision, yellow tinge to vision, appearance of halos around dark objects) are also relatively common.

Clonidine safety alert

Older Adult Patients Centrally acting alpha agonists (clonidine, guanabenz, guanfacine, methyldopa) and the adrenergic neuron-blocking agent reserpine have been designated as potentially inappropriate for use in geriatric patients due to their high risk of adverse CNS effects, bradycardia, and hypotension. Other drugs are recommended for first-line hypertension management in older-adult patients.

Prototype Drugs for Angina Pectoris

Organic Nitrates: -Nitroglycerin Beta Blockers: -Metoprolol -Propranolol Calcium Channel Blockers: -Nifedipine -Verapamil Drug That Increases Myocardial Efficiency: -Ranolazine

Phosphodiesterase Type 5 Inhibitors safety alert

PDE5 inhibitors—sildenafil [Viagra], tadalafil [Cialis], avanafil [Stendra], and vardenafil [Levitra]—are used for erectile dysfunction. All of these drugs can greatly intensify nitroglycerin-induced vasodilation. Life-threatening hypotension can result. Accordingly, concurrent use of PDE5 inhibitors with nitroglycerin is absolutely contraindicated.

HF Stage C

Patients in Stage C have symptoms of HF and also have structural heart disease. As discussed earlier, symptoms include dyspnea, fatigue, peripheral edema, and distention of the jugular veins. Treatment has four major goals: (1) relief of pulmonary and peripheral congestive symptoms, (2) improvement of functional capacity and quality of life, (3) slowing of cardiac remodeling and progression of LV dysfunction, and (4) prolongation of life. Treatment measures include those recommended for Stages A and B, plus those discussed in the sections that follow. Drug therapy: -Diuretics, ACE Inhibitors and ARBs, beta blockers, Aldosterone Antagonists, digoxin, Isosorbide Dinitrate/Hydralazine

HF Stage D

Patients in Stage D have advanced structural heart disease and marked symptoms of HF at rest, despite treatment with maximal dosages of medications used in Stage C. Repeated and prolonged hospitalization is common. For eligible candidates, the best long-term solution is a heart transplant. An implantable LV mechanical assist device can be used as a "bridge" in patients awaiting a transplant and to prolong life in those who are not transplant eligible. Management focuses largely on the control of fluid retention, which underlies most signs and symptoms. Intake and output should be monitored closely, and the patient should be weighed daily. Fluid retention can usually be treated with a loop diuretic, perhaps combined with a thiazide. If volume overload becomes severe, the patient should be hospitalized and given an IV diuretic. If needed, IV dopamine or IV dobutamine can be added to increase renal blood flow, thereby enhancing diuresis. Patients should not be discharged until a stable and effective oral diuretic regimen has been established. What about beta blockers and ACE inhibitors? These agents may be tried, but doses should be low and responses monitored with care. In Stage D, beta blockers pose a significant risk of making HF worse, and ACE inhibitors may induce profound hypotension or renal failure. When severe symptoms persist despite application of all recommended therapies, options for end-of-life care should be discussed with the patient and family.

Adverse Effects Related to Vasodilation

Postural Hypotension: Postural (orthostatic) hypotension is defined as a fall in blood pressure brought on by moving from a supine or seated position to an upright position. The underlying cause is relaxation of smooth muscle in veins. Because of venous relaxation, gravity causes blood to "pool" in veins, thereby decreasing venous return to the heart. Reduced venous return causes a decrease in cardiac output and a corresponding decrease in blood pressure. Reflex Tachycardia: Reflex tachycardia can be produced by dilation of arterioles or veins. The mechanism is this: (1a) arteriolar dilation causes a direct decrease in arterial pressure or (1b) venous dilation reduces cardiac output, which in turn reduces arterial pressure; (2) baroreceptors in the aortic arch and carotid sinus sense the drop in pressure and relay this information to the vasomotor center of the medulla; and (3) in an attempt to bring blood pressure back up, the medulla sends impulses along sympathetic nerves instructing the heart to beat faster. Expansion of Blood Volume: Prolonged use of arteriolar or venous dilators can cause an increase in blood volume (secondary to prolonged reduction of blood pressure). The increase in volume represents an attempt by the body to restore blood pressure to pretreatment levels.

A nurse is caring for a client who is taking spironolactone to treat hypertension. the nurse should recognize that which of the following client laboratory values requires immediate intervention?

Potassium 5.2 mEq/L

Statins nursing implications

Preadministration Assessment -Therapeutic Goal Statins, in combination with diet modification and exercise, are used primarily to lower levels of LDL cholesterol. -Baseline Data Obtain a baseline lipid profile, consisting of total cholesterol, LDL cholesterol, HDL cholesterol, and TGs (VLDLs). Also, obtain baseline LFTs and a CK level. -Identifying High-Risk Patients **Statins are contraindicated for patients with viral or alcoholic hepatitis and for women who are pregnant. **Exercise caution in patients with nonalcoholic fatty liver disease, in those who consume alcohol to excess, and in those taking fibrates or ezetimibe or agents that inhibit CYP3A4 (e.g., cyclosporine, erythromycin, ketoconazole, ritonavir). Use rosuvastatin with caution in Asian patients. Implementation: Administration -Route: Oral. -Administration: Instruct patients to take lovastatin with the evening meal; all other statins can be administered without regard to meals. Advise patients that dosing in the evening is preferred for all statins. Ongoing Evaluation and Interventions -Evaluating Therapeutic Effects Cholesterol levels should be monitored monthly early in treatment and at longer intervals thereafter. -Minimizing Adverse Effects Statins are very well tolerated. Side effects are uncommon, and serious adverse effects—hepatotoxicity and myopathy—are relatively rare.

clonidine nursing implications

Preadministration Assessment: -Therapeutic Goal Reduction of blood pressure in hypertensive patients.b -Baseline Data Determine blood pressure and heart rate. -Identifying High-Risk Patients Clonidine is embryotoxic to animals and should not be used during pregnancy. Rule out pregnancy before initiating treatment. Implementation: Administration -Routes Oral, transdermal. -Administration Oral. Advise the patient to take the major portion of the daily dose at bedtime to minimize daytime sedation. -Transdermal. Instruct the patient to apply transdermal patches to hairless, intact skin on the upper arm or torso, and to apply a new patch every 7 days. Ongoing Evaluation and Interventions -Evaluating Therapeutic Effects Monitor blood pressure. -Minimizing Adverse Effects *Drowsiness and Sedation. Inform patients about possible CNS depression and warn them to avoid hazardous activities if alertness is reduced. *Xerostomia. Dry mouth is common. Inform patients that discomfort can be reduced by chewing gum, sucking hard candy, and taking frequent sips of fluids. *Rebound Hypertension. Severe hypertension occurs rarely following abrupt clonidine withdrawal. Treat with a combination of alpha- and beta-adrenergic blockers. To avoid rebound hypertension, withdraw clonidine slowly (over 2 to 4 days). Inform patients about rebound hypertension and warn them against abrupt discontinuation of treatment. *Abuse. People who abuse cocaine, opioids, and other drugs frequently abuse clonidine as well. Be alert for signs of clonidine abuse (e.g., questionable or frequent requests for a prescription).

A nurse should identify that which of the following drugs is used only for the short-term treatment of a cardiac dysrhythmia because of the serious adverse effects associated with long-term use?

Procainamide

A nurse is teaching a client who has a new prescription for gemfibrozil. Which of the following instructions should the nurse include?

Report any new intolerance to fried foods report muscle tenderness expect periodic liver function testing

A nurse is caring for a client who has a depressive disorder and requires a prescription drug to treat hypertension. The nurse should recognize that which of the following antihypertensive drugs is contraindicated for this client?

Reserpine

A nurse is reviewing new prescriptions with a client who has heart disease. The nurse should instruct the client that which of the following drugs is prescribed to treat hypercholesterolemia?

Simvastatin

Sodium Nitroprusside preparations, dosage, and administration

Sodium nitroprusside [Nitropress] is available in powdered form (50 mg) to be dissolved and then diluted for IV infusion. Fresh solutions may have a faint brown color. Solutions that are deeply colored (blue, green, dark red) should be discarded. Nitroprusside in solution can be degraded by light, and hence should be protected with an opaque material. Blood pressure can be adjusted to practically any level by increasing or decreasing the rate of infusion. The initial infusion rate is 0.3 mcg/kg/min. The maximal rate is 10 mcg/kg/min. If infusion at the maximal rate for 10 minutes fails to produce an adequate drop in blood pressure, administration should stop. During the infusion, blood pressure should be monitored continuously, with either an arterial line or an electronic monitoring device. No other drugs should be mixed with the nitroprusside solution.

Nifedipine adverse effects

Some adverse effects are like those of verapamil; others are quite different. Like verapamil, nifedipine can cause flushing, dizziness, headache, peripheral edema, and gingival hyperplasia, and may pose a risk of chronic eczematous rash in older patients. -In contrast to verapamil, nifedipine causes very little constipation. Also, since nifedipine causes minimal blockade of calcium channels in the heart, the drug is not likely to exacerbate AV block, heart failure, bradycardia, or sick sinus syndrome. Accordingly, nifedipine is preferred to verapamil for patients with these disorders. --A response that occurs with nifedipine that does not occur with verapamil is reflex tachycardia. This response is problematic in that it increases cardiac oxygen demand and can thereby increase pain in patients with angina. To prevent reflex tachycardia, nifedipine can be combined with a beta blocker (e.g., metoprolol).

Mechanism of Antianginal Effects

Stable Angina. Nitroglycerin decreases the pain of exertional angina primarily by decreasing cardiac oxygen demand. Oxygen demand is decreased as follows: By dilating veins, nitroglycerin decreases venous return to the heart, and thereby decreases ventricular filling; the resultant decrease in wall tension (preload) decreases oxygen demand. In patients with stable angina, nitroglycerin does not appear to increase blood flow to ischemic areas of the heart. This statement is based on two observations. First, nitroglycerin does not dilate atherosclerotic coronary arteries. Second, when nitroglycerin is injected directly into coronary arteries during an anginal attack, it does not relieve pain. Both observations suggest that pain relief results from effects of nitroglycerin on peripheral blood vessels—not from effects on coronary blood flow. Variant Angina. In patients with variant angina, nitroglycerin acts by relaxing or preventing spasm in coronary arteries. Hence, the drug increases oxygen supply. It does not reduce oxygen demand.

Statins adverse effects

Statins are generally well tolerated. Side effects are uncommon. Some patients develop headache, rash, memory loss, or GI disturbances (dyspepsia, cramps, flatulence, constipation, abdominal pain). However, these effects are usually mild and transient. Serious adverse effects—hepatotoxicity and myopathy—are relatively rare. Some statins pose a greater risk than others, as noted here.

ACE inhibitors patient teaching

Take your medicine at least 1 hour before you eat, if you are taking captopril or moexipril, as described in the manufacturer's instructions, or 2 hours after you eat. You may take all other ACE inhibitors at any time, according to your healthcare provider's instructions.

methyldopa therapeutic use

The only indication for methyldopa is hypertension. Studies regarding methyldopa use in pregnant patients have shown improved outcomes ***without fetal harm, so the American Congress of Obstetricians and Gynecologists has designated methyldopa as a preferred drug in management of hypertension during pregnancy.

hemodynamic net effect of Nifedipine

The overall hemodynamic response to nifedipine is simply the sum of its direct effect (vasodilation) and indirect effect (reflex cardiac stimulation). Accordingly, nifedipine (1) lowers blood pressure, (2) increases heart rate, and (3) increases contractile force. Please note, however, that the reflex increases in heart rate and contractile force are transient and occur primarily with the IR formulation.

hemodynamic net effect of verapamil

The overall hemodynamic response to verapamil is the net result of (1) direct effects on the heart and blood vessels and (2) reflex responses. Because the direct effects of verapamil on the heart are counterbalanced by indirect effects, the drug has little or no net effect on cardiac performance: For most patients, heart rate, AV conduction, and contractility are not noticeably altered. Consequently, the overall cardiovascular effect of verapamil is simply vasodilation accompanied by reduced arterial pressure and increased coronary perfusion. ***same net effect with Diltiazem

Metroprolol therapeutic uses

The primary indication for metoprolol is hypertension. The drug is also approved for angina pectoris, heart failure, and myocardial infarction. IV administration is reserved for treatment of myocardial infarction.

Beneficial actions of HMG-CoA Reductase Inhibitors (Statins)

The statins have several actions that can benefit patients with (or at risk of) atherosclerosis. The most obvious and important are reductions of LDL cholesterol.

Verapamil and Diltiazem identifying high-risk patients

Verapamil and diltiazem are contraindicated for patients with severe hypotension, sick sinus syndrome (in the absence of electronic pacing), and second-degree or third-degree AV block. Use with caution in patients with heart failure or liver impairment and in patients taking digoxin or beta blockers.

ACE inhibitors therapeutic uses

When the ACE inhibitors were introduced, their only indication was hypertension. Today, they are also used for heart failure, acute MI, left ventricular (LV) dysfunction, and diabetic and nondiabetic nephropathy. In addition, they can help prevent MI, stroke, and death in patients at high risk for cardiovascular events. It should be noted that no single ACE inhibitor is approved for all of these conditions. However, given that all ACE inhibitors are very similar, it seems likely that all may produce similar benefits.

Statins drug and food interactions

With Other Lipid-Lowering Drugs: Combining a statin with most other lipid-lowering drugs (except probably the bile-acid sequestrants) can increase the incidence and severity of the most serious statin-related adverse events: muscle injury, liver injury, and kidney damage. The increase in risk occurs primarily with fibrates (gemfibrozil, fenofibrate), which are commonly combined with statins With Drugs That Inhibit CYP3A4: Drugs that inhibit CYP3A4 can raise levels of lovastatin and simvastatin substantially, and can raise levels of atorvastatin moderately, by slowing their inactivation. Important inhibitors of CYP3A4 include macrolide antibiotics (e.g., erythromycin), azole antifungal drugs (e.g., ketoconazole, itraconazole), HIV protease inhibitors (e.g., ritonavir), amiodarone (an antidysrhythmic drug), and cyclosporine (an immunosuppressant). If these drugs are combined with a statin, increased caution is advised. Some authorities recommend an automatic reduction in statin dosage if these inhibitors are used.

Gemfibrozil MOA

activates peroxisome proliferator-activated receptor alpha (PPAR) increasing synthesis of lipoprotein lipase and reducing production of apolipoprotein C-III to accelerate the clearance of very low density lipoproteins, and thereby reducing triglycerides

A nurse should recognize that milrinone is contraindicated for a client who has which of the following conditions?

acute myocardial infarction

A nurse is caring for a client who is taking amiodarone to treat A-Fib. which of the following should the nurse instruct the client to avoid while taking this drug?

grapefruit juice, can cause toxicity of potassium channel blockers, such as amiodarone

A nurse is teaching a client who has a new prescription for nitroglycerin. The nurse should instruct the client that which of the following manifestations is a potential adverse effect of the drug?

headache

Clonidine therapeutic uses

hypertension Suppression of sympathetic outflow decreases sympathetic stimulation of the heart and blood vessels.

Digoxin MOA

increases myocardial contractility by inhibiting sodium, potassium-ATPase ultimately preventing myocytes from restoring their proper ionic composition, producing calcium accumulation, and facilitating the interaction of myocardial contractile proteins: actin and myosin

Atorvastatin MOA

inhibits the hepatic enzyme, HMG CO-A Reductase from synthesizing cholesterol and ultimately causing hepatocytes to synthesize more LDL receptors - promoting the removal of LDLs from circulation. This drug also decreases the production of apolipoprotein B-100, lowering VLDLs and triglycerides

A nurse is providing teaching to a client who is taking simvastatin. The nurse should instruct the client to report which of the following manifestations as an indication of a serious adverse reaction that could require discontinuing drug therapy?

muscle pain

Carvedilol MOA

non-selectively blocks alpha-1 and beta-1 receptors to promote vasodilation, reduce heart rate and contractility, and suppress release of renin

Clonidine MOA

produces selective activation of alpha-2 receptors in the central nervous system, reducing sympathetic outflow to the blood vessels and the heart

Propranolol

prototype of the first-generation beta blockers, produces nonselective beta blockade. That is, this drug blocks both beta1- and beta2-adrenergic receptors. Propranolol was the first beta blocker to receive widespread clinical use and remains one of our most important beta-blocking agents.

a nurse is caring for a client who is taking a diuretic. the nurse should instruct the client to include which of the following foods in their diet to increase potassium intake?

raisins

Doxazosin MOA

selective competitive inhibitor of the alpha-1 adrenergic receptors causing vasodilation of arterioles and veins. Is in the same classification of medications used to treat BPH.

Metroprolol MOA

selectively blocks beta-1 receptors in the heart leading to reduced sympathetic outflow and suppression of renin activity

A nurse is caring for a client who has a glomerular filtration rate of 10/ mL/min and a reduced urine output. The nurse should clarify a prescription for hydrochlorothiazide for this client because of which of the following characteristics of the drug?

the drug does not promote diuresis for clients who have renal insufficiency

ACE inhibitors pharmacokinetics

• Nearly all ACE inhibitors are administered orally. The only exception is enalaprilat (the active form of enalapril), which is given IV. • Except for captopril and moexipril, all oral ACE inhibitors can be administered with food. • With the exception of captopril, all ACE inhibitors have prolonged half-lives, and hence can be administered just once or twice a day. Captopril is administered 2 or 3 times a day. • With the exception of lisinopril, all ACE inhibitors are prodrugs that must undergo conversion to their active form in the small intestine and liver. Lisinopril is active as given. • All ACE inhibitors are excreted by the kidneys. As a result, nearly all can accumulate to dangerous levels in patients with kidney disease, and hence dosages must be reduced in these patients. Only one agent—fosinopril—does not require a dosage reduction.

Digoxin key points

■ Digoxin and other inotropic agents increase the force of myocardial contraction and thereby increase cardiac output. ■ Of the available inotropic agents, digoxin is the only one that is both effective and safe when used orally and the only one suitable for long-term use. ■ Digoxin increases contractility by inhibiting myocardial Na+/K+-ATPase, thereby (indirectly) increasing intracellular calcium, which in turn facilitates the interaction of actin and myosin. ■ Potassium competes with digoxin for binding to Na+/K+-ATPase. Therefore, if potassium levels are low, excessive inhibition of Na+/K+-ATPase can occur, resulting in toxicity. Conversely, if potassium levels are high, insufficient inhibition can occur, resulting in therapeutic failure. Accordingly, it is imperative to keep potassium levels in the normal physiologic range: 3.5 to 5 mEq/L. ■ By increasing cardiac output, digoxin can reverse all of the overt manifestations of HF: cardiac output improves, heart rate decreases, heart size declines, constriction of arterioles and veins decreases, water retention reverses, blood volume declines, peripheral and pulmonary edema decrease, water weight is lost, and exercise tolerance improves. Unfortunately, although digoxin can improve symptoms, it does not prolong life. ■ In patients with HF, benefits of digoxin are not due solely to improved cardiac output; neurohormonal effects are important too. ■ Digoxin causes dysrhythmias by altering the electrical properties of the heart (secondary to inhibition of Na+/K+-ATPase). ■ The most common reason for digoxin-related dysrhythmias is diuretic-induced hypokalemia. ■ If a severe digoxin overdose is responsible for dysrhythmias, digoxin levels can be lowered using Fab antibody fragments [Digifab]. ■ In addition to dysrhythmias, digoxin can cause GI effects (anorexia, nausea, vomiting) and CNS effects (fatigue, visual disturbances). Gastrointestinal and CNS effects often precede dysrhythmias and therefore can provide advance warning of serious toxicity. ■ Digoxin has a narrow therapeutic range. ■ Digoxin is eliminated by renal excretion. ■ Although routine monitoring of digoxin levels is generally unnecessary, monitoring can be helpful when dosage is changed, symptoms of HF intensify, kidney function declines, signs of toxicity appear, or drugs that affect digoxin levels are added to or deleted from the regimen. ■ Maintenance doses of digoxin are based primarily on observation of the patient: Doses should be large enough to minimize symptoms of HF but not so large as to cause adverse effects. ■ Maintenance doses of digoxin must be reduced if renal function declines.

calcium channel blockers key points

▪ 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 heart rate, AV conduction, and myocardial contractility, so calcium channel blockade has the opposite effects. ▪ In the heart, calcium channels are coupled to beta1 receptors, activation of which enhances calcium entry. As a result, calcium channel blockade and beta blockade have identical effects on cardiac function. ▪ At therapeutic doses, nifedipine and the other dihydropyridines act primarily on VSM; in contrast, verapamil and diltiazem act on VSM and on the heart. ▪ All CCBs promote vasodilation, and hence are useful in hypertension and angina pectoris. ▪ Because they suppress AV conduction, verapamil and diltiazem are useful for treating cardiac dysrhythmias (in addition to hypertension and angina pectoris). ▪ Because of their cardiosuppressant effects, verapamil and diltiazem can cause bradycardia, partial or complete AV block, and exacerbation of heart failure. ▪ Beta blockers intensify cardiosuppression caused by verapamil and diltiazem. ▪ Nifedipine and other dihydropyridines can cause reflex tachycardia. Tachycardia is most intense with immediate-release formulations, and much less intense with sustained-release formulations. ▪ Beta blockers can be used to suppress reflex tachycardia caused by nifedipine and other dihydropyridines. ▪ Because they cause vasodilation, all CCBs can cause dizziness, headache, and peripheral edema. ▪ In toxic doses, nifedipine and other dihydropyridines can cause cardiosuppression, just like verapamil and diltiazem. ▪ Immediate-release nifedipine has been associated with increased mortality in patients with myocardial infarction and unstable angina, although a causal relationship has not been established. The National Heart, Lung, and Blood Institute recommends that immediate-release nifedipine, especially in higher doses, be used with great caution, if at all.