Ch 24 Heart Failure

Front 1

Catecholamines

Back 1

active amines (e.g., epinephrine, norepinephrine, dopamine) that have an effect on the cardiovascular system

Front 2

Decompensation

Back 2

the inability of the heart to adequately circulate oxygenated blood to the body’s vital organs

Front 3

Diastolic dysfunction

Back 3

impaired relaxation and filling of the ventricles during diastole

Front 4

Digitalis toxicity

Back 4

an accumulation of digitalis in the body that leads to nausea, vomiting, and atrial tachycardia

Front 5

Digitalization

Back 5

the administration of a loading dose of digoxin (Lanoxin) to achieve a therapeutic blood level of the medication more rapidly

Front 6

Endothelin

Back 6

a peptide that raises blood pressure, constricts blood vessels, and contributes to the onset of heart failure

Front 7

Inotropic

Back 7

related to or influencing the force of myocardial contractility

Front 8

Renin

Back 8

an enzyme produced by the kidney that divides angiotensinogen to form angiotensin I, which is then changed to angiotensin II to produce vasoconstriction

Front 9

Systolic dysfunction

Back 9

impaired myocardial contraction during systole

Front 10

Therapeutic index

Back 10

the blood level of a medication that will produce therapeutic effects

Front 11

Ventricular remodeling

Back 11

dilatation and hypertrophy of the ventricles in the initial phases of heart failure, causing the ventricle to assume a spherical shape

Front 12

Heart failure

Back 12

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.

Front 13

Heart failure

Back 13

________ 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.

Front 14

Endothelial dysfunction

Back 14

______________ 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.

Front 15

Hyperthyroidism

Back 15

___________ 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.

Front 16

Renal failure

Back 16

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).

Front 17

Heart failure

Back 17

______________ 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 ____________.

Front 18

Catecholamines

Back 18

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.

Front 19

Endothelin

Back 19

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.

Front 20

Hypoperfusion

Back 20

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.

Front 21

Arterial vasoconstriction

Back 21

_______________ 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.

Front 22

Right-sided

Back 22

_____________ 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.

Front 23

Right-sided

Back 23

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.

Front 24

Left-sided

Back 24

______________ 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.

Front 25

Left-sided

Back 25

____________ 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.

Front 26

Dyspnea & fatigue

Back 26

The cardinal manifestations of heart failure are __________ and _________, which can lead to exercise intolerance and fluid retention.

Front 27

asymptomatic

Back 27

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.

Front 28

Symptomatic

Back 28

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

Front 29

pulmonary edema

Back 29

Acute, severe cardiac decompensation is manifested by _______________, a medical emergency that requires immediate treatment.

Front 30

Right-Sided Heart FailureClinical Manifestations

Back 30

Edema of the lower extremities

Weight gain

Dyspnea

Fatigue

Hepatomegaly

Ascites

Anorexia

Nausea or abdominal pain

Front 31

Left-Sided Heart FailureClinical Manifestations

Back 31

Pulmonary congestion

Dyspnea with possible orthopnea

Cough

Audible crackles in the bases of the lung

Audible S3 or ventricular gallop

Front 32

Non-cardio risk factors

Back 32

§ Infections

§ Hyperthyroidism

§ Pulmonarydisease

§ Congenitalheart disease or defects

§ Excessiveparenteral fluids or blood transfusions

Front 33

Digoxin (Lanoxin)

Back 33

Inotropes (cardiac glycosides) prototype

Front 34

Hydrochlorothiazide (HCTZ)

Back 34

Thiazide diuretics prototype

Front 35

Enalapril maleate (Vasotec)

Back 35

Angiotensin-converting enzyme (ACE) inhibitors prototype

Front 36

Losartan potassium (Cozaar)

Back 36

Angiotensin II–receptor blockers (ARBs) prototype

Front 37

Propranolol (Inderal)

Back 37

Beta-adrenergic blocking agents prototype

Front 38

Beta-adrenergic blocking agents other drugs in class

Back 38

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)

Front 39

Spironolactone (Aldactone)

Back 39

Aldosterone antagonists aka Potassium sparing diuretic prototype

Front 40

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.

Back 40

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)

Front 41

Stage A

Back 41

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.

Front 42

Stage B

Back 42

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.

Front 43

Stage D

Back 43

Stage _: Patient presents with symptoms of heart failure. Most common symptoms noted include dyspnea, fatigue, peripheral edema, hepatomegaly with jugular vein distention, and ascites.

Front 44

Stage D

Back 44

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.

Front 45

Stage A recommendations

Back 45

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

Front 46

Stage B Recommendations

Back 46

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

Front 47

Stage C Recommendations

Back 47

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.

Front 48

Stage D Recommendations

Back 48

Stage ___ Recommendations

All therapies for stages A, B, and C

Permanent mechanical support with implantable defibrillators

Continuous inotropic therapy

Heart transplant

Hospice/palliative care

Front 49

Inotropes (cardiac glycosides)

Back 49

This drugs act to influence the contractility of the heart muscle.

Front 50

Inotropic

Back 50

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.

Front 51

Orally; elixir

Back 51

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.

Front 52

Orally; tablets

Back 52

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.

Front 53

Digoxin Route and dosage

Back 53

0.75–1.5 mg PO0.125–0.25 mg IV

Front 54

Digoxin Pregnancy category

Back 54

C

Front 55

Negative chronotropic

Back 55

In a patient with an atrial dysrhythmia, digoxin slows the rate of ventricular contraction (__________ ___________ effect)

Front 56

Digoxin Use

Back 56

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.

Front 57

Kidneys

Back 57

Digoxin is primarily excreted by the ___________, and the dosage should be reduced in the presence of renal impairment.

Front 58

Orally, IV

Back 58

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.

Front 59

Digoxin toxicity

Back 59

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.

Front 60

1 week

Back 60

It is important to note that when digoxin is discontinued, it takes approximately __ week for the drug to be eliminated from the body.

Front 61

Calcium

Back 61

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.