Cardiac/Vascular Nurse Exam Secrets Study Guide (23 page)

Both angiotensin-converting enzyme inhibitors and angiotensin II antagonists induce vasodilation. However, angiotensin II antagonists are more specific in their mechanism of action than angiotensin-converting enzyme inhibitors. These drugs are mainly used for the treatment of hypertension, but have other cardiovascular effects.

Adverse events associated with angiotensin-converting enzyme inhibitors include hypotension, glomerular damage, acute renal failure, hyperkalemia, dry cough, wheezing, angioedema, agranulocytosis, gastrointestinal upset, skin rash and/or other hypersensitivities.

Contraindications of angiotensin-converting enzyme inhibitors include women during their second and third trimester of pregnancy due to risk of fetal hypotension, anuria, renal failure, fetal malformations, and/or death.

Patients with renal insufficiency should not be prescribed angiotensin-converting enzyme inhibitors due to elimination through the kidneys. However, fosinopril and moexipril are not eliminated through the kidneys and therefore can be administered in this patient population. Hypotension, potassium levels, and renal function should be monitored in patients undergoing treatment with angiotensin-converting enzyme inhibitors.

Angiotensin II antagonists

Angiotensin II antagonists are more specific in action than angiotensin-converting enzyme inhibitors. Angiotensin II antagonists block angiotensin II receptors by inhibiting a subtype of the angiotensin II receptor known as AT
₁
. Angiotensin II antagonists do not interfere with bradykinin metabolism. The pharmacologic effect of angiotensin II antagonists is decreased blood pressure caused by a decrease in both peripheral resistance and blood volume. Inhibition of the AT
₁
receptors leads to inhibition of the pressor and aldosterone-releasing effects of angiotensin II, which causes the decrease in blood pressure.

Angiotensin II antagonists are mainly used to treat hypertension but have effects on other cardiovascular conditions.

Adverse events associated with angiotensin II antagonists include gastrointestinal upset, dry mouth, tooth pain, headache, dizziness, minor cough, dry skin and alopecia. Since angiotensin II antagonists do not impact bradykinin metabolism, angiotensin II antagonists present with limited cough and fewer side effects as compared to angiotensin-converting enzyme inhibitors. Angiotensin II antagonists provide a more specific approach to the treatment of hypertension as compared to angiotensin-converting enzyme inhibitors.

Contraindications associated with angiotensin II antagonists include pregnant women during their second and third trimesters due to risk of fetal malformations and death. Hypotension, potassium levels, and renal function should be monitored in patients undergoing treatment with angiotensin II antagonists.

Classes of agents included in the diuretic group of pharmacologic drugs

The classes of agents included in the diuretic group of pharmacologic agents include thiazide diuretics such as bendroflumethiazide, benzthiazide, chlorothiazide, chlorthalidone, hydrochlorothiazide, hydroflumethiazide, indapamide, methyclothiazide, metolazone, polythiazide, quinethazone and trichlormethiazide; loop diuretics such as bumetanide, ethacrynic acid, furosemide and torsemide; potassium-sparing diuretics such as amiloride, spironolactone, and triamterene; and osmotic diuretics such as glycerin and mannitol.

Diuretics prevent reabsorption of sodium in the kidneys, with each class of diuretic working on a slightly different site within the nephron of the kidney. Each of these classes of diuretics has a slightly different mechanism of action.

Thiazide diuretics

Therapeutic uses for thiazide diuretics include treatment of congestive heart failure, hypertension, and edema. The most common adverse effects associated with thiazide diuretics include electrolyte imbalance, fluid imbalance, hypotension, oliguria, anuria, dizziness, hypokalemia, hyponatremia, hypocalcemia, hyperglycemia, hyperuricemia, and gastrointestinal upset.

Contraindications of thiazide diuretics include patients with renal disease, hypokalemia, dysrhythmia, glucose intolerance, and gout. Thiazide diuretics should not be used prior to bedtime due to increase urine output. Caution should be used when using diuretics in combination with other antihypertensive agents. Practicing clinicians need to monitor electrolyte and renal function to prevent complications. Additionally, patients should monitor potassium intake due to potential for electrolyte imbalance and supplement accordingly.

Thiazide diuretics prevent the reabsorption of sodium within the nephron of the kidneys, which allow for sodium and other ions to be excreted in the urine and not reabsorbed in the blood stream. Specifically, thiazide diuretics inhibit sodium and chloride reabsorption in the nephron, resulting in excretion of potassium, chloride, and sodium in the urine. The excretion of sodium in the urine decreases the glomerular filtration rate and has been associated with moderate potassium loss, which needs to be monitored. Thiazide diuretic net effect is to decrease blood pressure, decrease cardiac stroke volume, and cardiac output.

Loop diuretics

Loop diuretics prevent the reabsorption of sodium and chloride within the nephron of the kidneys, which allow for sodium, chloride, and potassium to be excreted in the urine and not reabsorbed in the blood stream. Loop diuretics are more powerful than thiazide diuretics and are associated with increased potassium loss. Loop diuretic net effect is to decrease blood pressure, cardiac stroke volume, and cardiac output.

Therapeutic uses of loop diuretics include treatment of congestive heart failure, pulmonary edema, hypertension, and edema associated with congestive heart failure, renal disease, or liver disease.

The most common adverse effects associated with loop diuretics include electrolyte imbalance, fluid imbalance, hypotension, oliguria, anuria, dizziness, hypokalemia, hyponatremia, hypocalcemia, hyperglycemia, hyperuricemia, ototoxicity resulting from hearing loss, and gastrointestinal upset.

Contraindications of loop diuretics include patients with renal disease, hypokalemia, dysrhythmia, glucose intolerance, and gout. Loop diuretics should not be used prior to bedtime due to increased urine output. Caution should be used when using diuretics in combination with other antihypertensive agents. Practicing clinicians need to monitor electrolyte and renal function to prevent complications. Additionally, patients should monitor potassium intake due to potential for electrolyte imbalance and supplement accordingly.

Potassium-sparing diuretics

Potassium-sparing diuretics increase sodium excretion and decrease potassium secretion in the nephron of the kidneys, which allow for sodium and other ions to be excreted in the urine and not reabsorbed in the blood stream. However, potassium-sparing diuretics are associated with decreased potassium excretion compared to thiazide and loop diuretics, making potassium-sparing diuretics an attractive option. Potassium-sparing diuretics’ net effect is to decrease blood pressure, decrease cardiac stroke volume, and cardiac output.

Therapeutic uses of potassium-sparing diuretics include hypertension and edema from congestive heart failure, renal disease, or liver disease. In patients undergoing treatment with thiazide or loop diuretics who develop hypokalemia, potassium-sparing diuretics are another option.

The most common adverse effects associated with potassium-sparing diuretics include electrolyte imbalance, fluid imbalance, hypotension, oliguria, anuria, dizziness, hyperkalemia, some hyponatremia, glucose intolerance in diabetic patients, gynecomastia, and gastrointestinal upset.

Potassium-sparing diuretics should not be used prior to bedtime due to increased urine output. Caution should be used when using diuretics in combination with other antihypertensive agents. Practicing clinicians need to monitor electrolyte and renal function to prevent complications. Additionally, patients should monitor potassium intake due to potential for electrolyte imbalance and supplement accordingly, even though potassium levels are not impacted to the same degree as with thiazide or loop diuretics.

Osmotic diuretics

Osmotic diuretics prevent the reabsorption water within the permeable regions of the nephron because these nonabsorbable agents create an osmotic gradient favoring increased urine volume. Osmotic diuretic net effect is to decrease blood pressure, decrease cardiac stroke volume, and cardiac output.

Therapeutic uses of osmotic diuretics include treatment of intracranial pressure and brain edema. The most common adverse effects associated with osmotic diuretics include electrolyte imbalance, fluid imbalance, hypotension, oliguria, anuria, and dizziness.

Osmotic diuretics should not be used prior to bedtime due to increased urine output. Caution should be used when using diuretics in combination with other antihypertensive agents. Practicing clinicians need to monitor electrolyte and renal function to prevent complications. Additionally, patients should monitor potassium intake due to potential for electrolyte imbalance and supplement accordingly.

Classes of agents included in the antihyperlipidemic group of pharmacologic drugs

The classes of agents included in the antihyperlipidemic group of pharmacologic drugs include resins, niacin, statins, also known as HMG-coenzyme A reductase inhibitors, and fibric acid derivatives. Drugs within the resin class of agents include cholestyramine, colestipol, and colesevelam. Drugs within the statins, or HMG-coenzyme A reductase inhibitors, include atorvastatin, pravastatin, fluvastatin, simvastatin and lovastatin. Drugs within the fibric acid derivatives include clofibrate, fenofibrate, and gemfibrozil.

Antihyperlipidemic classes of agents directly or indirectly affect lipid and cholesterol levels by lowering low-density lipid levels, increasing high-density lipid levels and decreasing triglyceride levels.

Resins

The pharmacologic effects of resins include decrease in low-density lipid levels, increase in high-density lipid levels and decrease in triglyceride levels. The mechanism of action of these agents is to act as bile acid sequestrants, which increase liver low-density lipoprotein receptors, removing low-density lipids from circulation and oxidizing the cholesterol from low-density lipids to form bile acids.

Therapeutic uses for resins include treatment of hypercholesterolemia and hyperlipidemia. Resins are recommended only when a patient fails first line therapy with diet modifications and exercise and their low-density lipid levels are above 160 mg/dL or above 130 mg/dL with more than 2 cardiovascular risk factors such as obesity, smoking or high-density lipid levels below 40 mg/dL. The goal of treatment when prescribing resins in patients with coronary heart disease or at high risk for coronary heart disease is low-density lipid levels below 100 mg/dL. Resins may also be used in children between the ages of 11 and 20.

Adverse effects associated with resins include gastrointestinal upset, bloating, constipation, and malabsorption of vitamins A, D, and K. Contraindications associated with resins include hypertriglyceridemia, biliary obstruction, abnormal intestinal function, pregnancy, and lactation.

Practicing clinicians should inform patients that these agents should not be taken in dry powder form, but mixed with fluids to be efficacious. Additionally, if prescribed resins in tablet form, the tablets should not be cut, chewed, or crushed, as they will become ineffective if that is done. Resins are designed to be broken down in the gastrointestinal tract and, if broken down sooner, the drugs will become ineffective.

Niacin

The pharmacologic effects of niacin include a decrease in low-density lipid levels, increase in high-density lipid levels and decrease in triglyceride levels. The mechanism of action of niacin is inhibition of lipolysis of triglycerides in fatty tissue, which decreases synthesis of triglycerides in the liver. In turn, decreased triglyceride synthesis decreases low-density lipid synthesis, decreasing low-density lipid levels. Niacin is the most effective agent for increasing high-density lipid levels, but also has effects on lowering low-density lipid levels and triglyceride levels.

Therapeutic uses include hypertriglyceridemia, hypercholesterolemia, and hyperlipidemia. Niacin is recommended only when a patient fails first line therapy with diet modifications and exercise and their low-density lipid levels are above 160 mg/dL or above 130 mg/dL with more than 2 cardiovascular risk factors such as obesity, smoking or high-density lipid levels below 40 mg/dL. The goal of treatment when prescribing niacin in patients with coronary heart disease or at high risk for coronary heart disease is low-density lipid levels below 100 mg/dL.

Adverse events associated with niacin include flushing, pruritus, abnormal glucose tolerance, and hyperuricemia. The most common adverse events associated with niacin include flushing and dyspepsia. These common adverse events decrease patient compliance and effectiveness of niacin treatment. However, flushing tends to decrease with treatment duration. Patients may also take aspirin 30 minutes prior to taking niacin to reduce flushing. They may also reduce hot beverage or alcohol intake to reduce extent and degree of flushing.

Contraindications associated with niacin treatment include pregnancy and gout. Patients should not take oral nicotinamide as treatment for hypertriglyceridemia, hypercholesterolemia, and hyperlipidemia because this source of niacin does not have any impact on lipid levels. The effective dose for antihypertensive treatment ranges between 1 and 2 grams per day or more.