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61 Cards in this Set
- Front
- Back
Catecholamines |
active amines (e.g., epinephrine, norepinephrine, dopamine) that have an effect on the cardiovascular system |
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Decompensation |
the inability of the heart to adequately circulate oxygenated blood to the body’s vital organs |
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Diastolic dysfunction |
impaired relaxation and filling of the ventricles during diastole |
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Digitalis toxicity |
an accumulation of digitalis in the body that leads to nausea, vomiting, and atrial tachycardia |
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Digitalization |
the administration of a loading dose of digoxin (Lanoxin) to achieve a therapeutic blood level of the medication more rapidly |
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Endothelin |
a peptide that raises blood pressure, constricts blood vessels, and contributes to the onset of heart failure |
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Inotropic |
related to or influencing the force of myocardial contractility |
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Renin |
an enzyme produced by the kidney that divides angiotensinogen to form angiotensin I, which is then changed to angiotensin II to produce vasoconstriction |
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Systolic dysfunction |
impaired myocardial contraction during systole |
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Therapeutic index |
the blood level of a medication that will produce therapeutic effects |
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Ventricular remodeling |
dilatation and hypertrophy of the ventricles in the initial phases of heart failure, causing the ventricle to assume a spherical shape |
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Heart failure |
a complex clinical condition that occurs when the heart cannot pump enough blood to meet the body tissue’s needs for oxygen and nutrients. It can result from impaired myocardial contraction, systolic and/or diastolic dysfunction. It can result in an accumulation of fluid in the lungs and peripheral tissues. |
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Heart failure |
________ is caused by various conditions that prevent the contractile myocardial cells and the endothelial cells that line the heart and blood vessels from functioning properly. Hypertension, cardiomyopathy, and acute myocardial infarction can affect myocardial or endothelial cell function, leading to ___________. It can also be caused by volume overload, renal failure, or hypermetabolic states. |
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Endothelial dysfunction |
______________ promotes processes that can lead to narrowing of the blood vessel lumen, such as the accumulation of atherosclerotic plaque, abnormal cell growth, inflammation, or platelet activation. The narrowing of the lumen can lead to blood clot formation and vasoconstriction. These are the major factors in coronary artery disease and hypertension and the most common conditions that lead to heart failure. |
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Hyperthyroidism |
___________ is a hypermetabolic condition that is a major causative factor in the development of heart failure. Thyroid function is increased, which causes an increase in heart rate and myocardial contractility and ultimately cardiac output. The patient is prone to heart failure due to the increased cardiac output. |
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Renal failure |
Fluid volume overload impairs the pumping ability of the heart, contributing to the development of heart failure. Fluid volume overload can occur in patients with _____________. Fluid volume overload can also be caused by the excessive administration of intravenous (IV) fluids or blood transfusions, or therapy with certain medications such as corticosteroids, estrogens, and nonsteroidal anti-inflammatory agents (which promote sodium and water retention). |
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Heart failure |
______________ results in low cardiac output and inadequate filling of the arteries. As a result, the neurohormonal system activates several feedback mechanisms. The baroreceptors in the aortic arch and carotid sinus that normally inhibit sympathetic nervous system activity are blunted in the patient who is experiencing ____________. |
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Catecholamines |
The circulating ______________ increase the force of myocardial contractility, as does the increased activity of the sympathetic nervous system. The patient’s heart rate increases, and the blood vessels constrict. Levels of endothelin, a peptide secreted by the endothelial cells, are increased in heart failure. |
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Endothelin |
a peptide secreted by the endothelial cells, are increased in heart failure. It is a potent vasoconstrictor and may exert direct toxic effects on the heart. |
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Hypoperfusion |
Patients with severe heart failure have constriction of the arterioles in the cerebral, myocardial, renal, hepatic, and mesenteric vascular beds. This results in increased organ ______________ and dysfunction. |
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Arterial vasoconstriction |
_______________ impairs cardiac function by increasing the resistance (afterload) against which the ventricle ejects blood. This increases the filling pressures inside the heart, which in turn, increases the stress on the heart by stretching the walls of the heart muscle, predisposing the patient to subendocardial ischemia. |
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Right-sided |
_____________ heart failure results from an accumulation of blood in the systemic venous system. There are two pumps within the heart. The _____________ pump pumps unoxygenated blood from the systemic circulation into the pulmonary circulation. Failure of the _____________ pump results in an increase in the _____ atrial, ______ ventricular, end-diastolic, and systemic venous pressures. |
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Right-sided |
The causes of ___________ heart failure are stenosis or regurgitation of the pulmonic or tricuspid valves, ____________ ventricular infarction, cardiomyopathy, or recurrent left-sided heart failure. In some cases severe pneumonia, pulmonary embolus, or pulmonary hypertension can result in ___________ heart failure. |
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Left-sided |
______________ heart failure results in a decrease in cardiac output related to an increase in _______ atrial and ________ ventricular end-diastolic pressures and congestion in the pulmonary circulation. The ________ side of the heart normally moves blood from the low-pressure pulmonary circulation to the higher pressure arterial side of the systemic circulation. |
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Left-sided |
____________ heart failure is most commonly caused by a myocardial infarction or cardiomyopathy. The patient experiences pulmonary edema at night while supine in bed because the _______ ventricle cannot pump the blood effectively out of the ventricle into the aorta and the systemic circulation. The pressure in the ________ atrium increases, resulting in decreased blood flow from the pulmonary vessels. The increase in pulmonary venous pressure forces fluid from the pulmonary capillaries into the alveoli, impairing gas exchange. |
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Dyspnea & fatigue |
The cardinal manifestations of heart failure are __________ and _________, which can lead to exercise intolerance and fluid retention. |
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asymptomatic |
Patients with compensated or ____________ heart failure usually have no symptoms at rest and no edema. In these patients, dyspnea and fatigue occur only with activities that require moderate- to high-level exertion.
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Symptomatic |
Patients with ___________ heart failure have symptoms that occur with minimal exertion or at rest, ankle edema, and distention of the jugular vein. These signs and symptoms reflect decompensation
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pulmonary edema |
Acute, severe cardiac decompensation is manifested by _______________, a medical emergency that requires immediate treatment. |
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Right-Sided Heart FailureClinical Manifestations |
Edema of the lower extremities Weight gain Dyspnea Fatigue Hepatomegaly Ascites Anorexia Nausea or abdominal pain |
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Left-Sided Heart FailureClinical Manifestations |
Pulmonary congestion Dyspnea with possible orthopnea Cough Audible crackles in the bases of the lung Audible S3 or ventricular gallop |
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Non-cardio risk factors |
§ Infections § Hyperthyroidism § Pulmonarydisease § Congenitalheart disease or defects § Excessiveparenteral fluids or blood transfusions |
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Digoxin (Lanoxin) |
Inotropes (cardiac glycosides) prototype |
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Hydrochlorothiazide (HCTZ) |
Thiazide diuretics prototype |
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Enalapril maleate (Vasotec) |
Angiotensin-converting enzyme (ACE) inhibitors prototype |
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Losartan potassium (Cozaar) |
Angiotensin II–receptor blockers (ARBs) prototype |
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Propranolol (Inderal) |
Beta-adrenergic blocking agents prototype |
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Beta-adrenergic blocking agents other drugs in class |
Acebutolol hydrochloride (Monitan) Atenolol (Tenormin) Betaxolol hydrochloride (Kerlone) Bisoprolol fumarate (Zebeta) Carteolol hydrochloride (Cartrol, Ocupress) Carvedilol (Coreg) Esmolol hydrochloride (Brevibloc) Labetalol hydrochloride (Trandate) Metoprolol tartrate (Lopressor, Toprol XL) Nadolol (Corgard) Penbutolol (Levatol) Pindolol (Visken) Sotalol (Betapace) |
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Spironolactone (Aldactone) |
Aldosterone antagonists aka Potassium sparing diuretic prototype |
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A patient who has had an acute myocardial infarction is at risk for developing left-sided heart failure. If the patient takes nonsteroidal anti-inflammatory agents, such as ibuprofen (Motrin) routinely, this may increase the risk of developing left-sided heart failure due to the retention of sodium. |
A patient is diagnosed with acute myocardial infarction. Which of the following medications will precipitate the development of left-sided heart failure in this patient? ibuprofen (Motrin) furosemide (Lasix) gabapentin (Neurontin) fexofenadine (Allegra) |
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Stage A |
Stage _: Patient presents without signs and symptoms of heart failure but is placed at high risk for the development of heart failure. Patients at risk for developing heart failure are those with hypertension, diabetes, history of alcohol abuse, family history of cardiomyopathy, or past history of treatment with chemotherapeutic agents. |
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Stage B |
Stage _: Patient presents without signs and symptoms of heart failure but has structural cardiac changes that place the patient at risk for heart failure. The structural changes most often associated with Stage B are past myocardial infarction, left ventricular hypertrophy, and valvular disorders of the heart. |
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Stage D |
Stage _: Patient presents with symptoms of heart failure. Most common symptoms noted include dyspnea, fatigue, peripheral edema, hepatomegaly with jugular vein distention, and ascites. |
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Stage D |
Stage _: The patient presents with debilitating symptoms of heart failure at rest. The patient has symptoms related to advanced heart disease and requires aggressive treatment. |
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Stage A recommendations |
Stage ____ Recommendations Smoking cessation Alcohol avoidance Treatment of hypertension with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) Control of blood glucose levels |
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Stage B Recommendations |
Stage ____ Recommendations Smoking cessation Alcohol avoidance Treatment with an ARB Treatment with an ACE inhibitor and beta blocker Valve replacement or repair for patients with hemodynamically significant valvular stenosis or regurgitation Implantable defibrillator if indicated |
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Stage C Recommendations |
Stage ____ Recommendations Smoking cessation Alcohol avoidance Sodium restriction Treatment with an inotrope (cardiac glycoside) Treatment with diuretics Treatment with ACE inhibitors and beta-blockers If ACE inhibitors are not tolerated due to cough, treatment is with ARBs such as valsartan (Diovan) or candesartan cilexetil (Atacand). Nonsteroidal anti-inflammatory agents, antidysrhythmic agents, and calcium channel blockers should not be used. |
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Stage D Recommendations |
Stage ___ Recommendations All therapies for stages A, B, and C Permanent mechanical support with implantable defibrillators Continuous inotropic therapy Heart transplant Hospice/palliative care |
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Inotropes (cardiac glycosides) |
This drugs act to influence the contractility of the heart muscle. |
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Inotropic |
This means related to, or influencing the force of, myocardial contractility.) Digoxin (Lanoxin) is the prototype drug of this class. Digoxin is derived from the digitalis plant. It is used to treat heart failure, atrial fibrillation, and atrial flutter. |
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Orally; elixir |
There are various preparations of digoxin. It is primarily given ______ either as a tablet or elixir. The ______ is absorbed more effectively than the tablet and is used primarily with infants and children. |
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Orally; tablets |
When digoxin is given ______, absorption varies among available preparations. With _______, the most frequently used formulation, differences in bioavailability are important because a person who is stabilized on one formulation may be underdosed or overdosed if another formulation is administered. |
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Digoxin Route and dosage |
0.75–1.5 mg PO0.125–0.25 mg IV |
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Digoxin Pregnancy category |
C |
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Negative chronotropic |
In a patient with an atrial dysrhythmia, digoxin slows the rate of ventricular contraction (__________ ___________ effect) |
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Digoxin Use |
management of heart failure, atrial fibrillation, and atrial flutter. ____________ is administered to patients with acute or chronic conditions, patients who are being digitalized, or for maintenance therapy. |
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Kidneys |
Digoxin is primarily excreted by the ___________, and the dosage should be reduced in the presence of renal impairment. |
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Orally, IV |
When given ________, the onset of action occurs in 30 minutes to 2 hours, with the peak effect of the medication occurring in approximately 6 hours. When digoxin is given parenterally through the __________ route, the onset of action occurs within 10 to 30 minutes and reaches a peak effect in 1 to 5 hours. |
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Digoxin toxicity |
the nurse must be alert to signs and symptoms of _________, which include very slow or very rapid ventricular rhythm, nausea, vomiting, loss of appetite, abdominal distention, blurred vision, and mental changes. During rapid digitalization, the patient is monitored continuously on a cardiac monitor. |
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1 week |
It is important to note that when digoxin is discontinued, it takes approximately __ week for the drug to be eliminated from the body. |
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Calcium |
Digoxin increases the force of myocardial contractility by inhibiting sodium, potassium, adenosine triphosphatase (Na, K-ATPase), an enzyme in cardiac cell membranes that decreases the movement of sodium out of myocardial cells after contraction. As a result, calcium enters the cell in exchange for sodium, causing additional ___________ to be released from intracellular binding sites and increasing myocardial contractility. |