Too Pooped to Pump

28 Nursing made Incredibly Easy! January/February 2006

Too poopedto pump

Managing chronic

January/February 2006 Nursing made Incredibly Easy! 29

The body dependson the heart’sability to circulate

blood. When the heart is damaged by illness or injury, the body marshals allof its forces to make up for the loss of function. This article examines whathappens when heart failure overcomes the body’s ability to compensate, andoffers insights on treatments that can help fix the problem.JANET RIGGS, RN, CCRN, CCNS, MSNResearch Project Manager for Heart Failure Clinical TrialsDepartment of Cardiology • Penn Presbyterian Medical Center • Philadelphia, Pa.

The author has disclosed that she has no significant relationships with or financial interest in any commercial companies that pertain to this educational activity.

BEA SINGER, age 67, awakens with astart from a sound sleep, gasping. She sitsup, trying to catch her breath, and shakesher husband awake. “Harry! Fix my pil-lows!” Just as he has every night for thepast week, he fetches three pillows andarranges them behind her back to propher up. Then he puts a finger under herchin and looks hard into her frightenedeyes. “That’s it, Bea. We’re going to thehospital.”

He’d said it before, and each time she’dpooh-poohed the idea, but tonight it’s differ-ent. She can’t catch her breath even sittingup, so she lets him help her into her coat andout to the car. She’s so tired she just wants tosit down.

When she’s examined at the local hospi-tal’s emergency department (ED), Mrs.Singer’s oxygen saturation (SaO2) is 89% onroom air and 95% on 3 L of nasal oxygen.Vital signs include heart rate, 116 and irregu-lar; respirations, 42; and blood pressure,102/74. Lung auscultation reveals bilateralcrackles halfway up. Her first and secondheart sounds (S1 and S2) are soft, and she hasan S3 heart sound. She has 2+ pitting edemain her legs, and her liver border is two fin-

gerbreadths below the lowest right rib. Herjugular venous pressure is 8 cm above thesternal angle.

Mrs. Singer’s medical history is positivefor an anterior wall myocardial infarction(MI) 5 years before. She’s been under treat-ment for the past 2 years for New YorkHeart Association (NYHA) Class II heartfailure. Her history is negative for smoking,reactive airway disease, cancer, renal insuffi-ciency, and diabetes. Her father died of anMI when he was 65; her mother died ofbreast cancer 20 years ago at age 66.

So what’s behind Mrs. Singer’s increasingbreathlessness?

Winding downMrs. Singer presented at the ED with thecardinal signs of heart failure: dyspnea, fa-tigue, and fluid retention. She’s among thegrowing number of patients diagnosedwith the condition, which is fast becomingone of our most important health care is-sues. Hospitalizations for heart failure areincreasing, in part due to incomplete treat-ment during hospitalization, poor applica-tion of chronic heart failure managementguidelines, and patient nonadherence to

2.5ANCC/AACN

CONTACT HOURS

heart failure

treatment recommen-dations. And whenyou consider that mil-

lions of baby boomersare now in their 50s and

60s, and more people are sur-viving longer after a heart attack, it’s easyto see why in the next decade, the numberof individuals with heart failure will con-tinue to grow rapidly (see Heart failure bythe numbers).

According to the National Institutes ofHealth, about 20% of patients with heart fail-ure will die within a year of diagnosis; two-thirds will die within 5 years. The AmericanHeart Association (AHA) says that 80% ofmen and 70% of women under age 65 withheart failure will die within 8 years. Qualityof life is adversely affected; patients withheart failure are at increased risk for depres-sion.

In this article, I’ll discuss what’s beingdone to improve these outcomes. But firstlet’s see what happens to the body in heartfailure.

Get me some air!In heart failure, the heart can’t supply suffi-cient quantities of blood and oxygen tomeet the metabolic needs of the body’s tis-

sues. It begins withsome type of injuryto the myocardiumthat impairs theability of the ventri-cles to fill with or toeject blood. This in-jury may result indilatation and/orhypertrophy of oneor both ventricles, aprocess called re-modeling. Remodel-ing of the ventriclesprogresses overtime; the patientmay remain asymp-tomatic for months

or even years. Inevitably, however, signsand symptoms will appear and worsenwithout treatment.

There are different types of heart failure.In low output heart failure, the left ventriclecan’t eject a normal volume of blood due toweakness of the left ventricular muscle sec-ondary to MI or cardiomyopathy, low flowcoming from an impaired right ventricle, oraortic valve stenosis. Causes of impairedright ventricular function include MI or anextrinsic insult like pulmonary hyperten-sion.

High output heart failure occurs when thevolume of blood exceeds what the left ven-tricle can eject. The cardiac output remainshigh for a while, until the pressure of thehigh blood volume causes dilatation of theventricle and a backup of fluid into the pul-monary interstitial spaces. Mitral valveregurgitation, aortic valve insufficiency,hyperthyroidism, anemia, and hypervolemiafrom an extrinsic cause (such as excess intra-venous [I.V.] fluid administration) are associ-ated with high-output heart failure.

Biventricular failure can occur when back-up pressures from the failing left ventricleresult in dilatation and failure in the rightventricle.

Another important distinction in the clas-sification of heart failure involves systolicdysfunction versus diastolic dysfunction.Left ventricular systolic dysfunction occurswhen the heart muscle is too weak to con-tract fully. As a result, a reduced volume ofblood leaves the ventricles during systolicejection. In normal heart function, 60% to80% of the blood contained in the left ventri-cle is ejected with each beat; this is called theejection fraction.

Left ventricular diastolic dysfunction occurswhen the left ventricle has increased dias-tolic stiffness (reduced compliance) and can’tfill adequately at normal diastolic pressures.The elevated pressures needed for fillingcause signs and symptoms of pulmonarycongestion. A person with left ventriculardiastolic dysfunction typically has a normal


Heart failure by the numbersIn the United States, there are about 5 millionpeople with heart failure, and more than550,000 new cases are diagnosed each year,according to the American College ofCardiology/American Heart Association. Heartfailure prompts 12 to 15 million office visits and6.5 million hospital days each year. During thelast 10 years, the annual number of hospitaliza-tions for heart failure as a primary diagnosishas increased to over 1 million, at a cost toMedicare and third-party payers of about $24.3billion. Around 55,000 Americans are predictedto die of heart failure in 2006.

No matterwhat you call it,this is killing me!

or high ejection fraction. Because the contrac-tility of the muscle isn’t impaired, the normalamount of blood is ejected from the ventriclewith each beat. Long-standing untreated sys-temic hypertension causes cardiac musclehypertrophy, which can lead to this type ofdiastolic dysfunction.

Coronary artery disease is responsible forabout two-thirds of all cases of heart failure.The remainder of cases are characterized bynonischemic cardiomyopathy. Among themany causes of nonischemic cardiomyopa-thy are systemic hypertension, thyroid dys-function, valvular heart disease, and expo-sure to cardiotoxic substances like alcohol,cocaine, or chemotherapeutic agents.Frequently, the cause is unknown; this isreferred to as idiopathic dilated cardiomy-opathy.

On stageHeart failure is a progressive disease. Awidely used staging system that empha-sizes the development and progression ofthe disease was jointly developed by theAmerican College of Cardiology (ACC)and the AHA. It classifies patients as fol-lows:■ Stage A identifies patients at risk of de-veloping heart failure who don’t have anystructural heart disease or symptoms ofheart failure. Some types of patientswhom you may see with Stage A heartfailure include those with diabetes, coro-nary artery disease, or hypertension.■ Stage B describes patients with docu-mented structural changes who don’t yethave signs or symptoms of heart failure.Some types of patients whom you may seewith Stage B heart failure are those with ahistory of MI, those with valve regurgita-tion on echocardiogram, or those with leftventricular hypertrophy on a 12-lead elec-trocardiogram (ECG). These patients havea documented structural change to theirheart, but they don’t yet demonstratesymptoms of heart failure.■ Stage C refers to patients who have

structural changes and who have or havehad symptoms.■ Stage D describes patients with refrac-tory heart failure who may need mechani-cal or pharmaceutical support, a hearttransplant, or end-of-life care.

Patients classified as Stage A, althoughasymptomatic, are treated to reduce theirrisk for developing heart failure; the goal isto help them achieve longer survival withbetter quality.

Next, I’ll explain the NYHA functionalclassification system.

New York, New YorkThe ACC/AHA guideline staging sys-tem was developed to complement theNYHA functional classification system,which primarily gauges the severity ofsymptoms.■ Class I: Ordinary physical activitydoesn’t cause undue fatigue, dyspnea, oranginal pain.■ Class II: The patient has slight limita-tion of physical activity but is asympto-matic at rest. Ordinary physical activitycauses fatigue, palpitations, dyspnea, oranginal pain.■ Class III: The patient has marked limi-tation of physical activity but is typicallyasymptomatic at rest. Less than ordinaryphysical activity causes fatigue, palpita-tions, dyspnea, or anginal pain.■ Class IV: The patient can’t perform anylevel of physical activity without discom-fort; symptoms may be present at rest.Discomfort increases with physical activ-ity. This patient will be considered formechanical support, continuous pharma-ceutical support, transplant, or end-of-lifecare.

Now, let’s see how the heart tries to makeup for its inability to pump up to par in leftventricular systolic dysfunction.

Release the vasoconstrictors!Compensated heart failure occurs whenthe heart is injured (such as by an MI) or


All theworld’s a

stage whenyour patient

has heartfailure.


becomes diseased (such as with viral my-ocarditis). The body launches several com-pensatory mechanisms to maximize thefunctioning of the heart, which has begunto pump less efficiently. One of thesemechanisms stimulates the sympatheticnervous system to release norepinephrineand epinephrine, increasing the heart rateand thus improving cardiac output. Usu-ally, anytime the heart rate is increased,cardiac output will also increase, accord-ing to the equation cardiac output = strokevolume x heart rate.

Another compensatory mechanism is theactivation of the renin-angiotensin-aldos-terone system that occurs when kidneyperfusion decreases. Renin convertsangiotensinogen to angiotensin I, which isconverted into angiotensin II in the lungs byangiotensin-converting enzyme (ACE).Angiotensin II is a powerful vasoconstrictor.This mechanism increases fluid volume andmaintains blood pressure. The rise in bloodpressure causes increased resistance (orincreased afterload) against ventricular ejec-tion, eventually causing ventricular hyper-trophy. Aldosterone increases the reabsorp-tion of sodium and water in the kidneys,which in turn raises blood pressure.

The increase in angiotensin II also stimu-lates the release of vasopressin, or antidiuret-ic hormone, from the posterior pituitarygland. Vasopressin is another powerfulvasoconstrictor, and it promotes renalrelease of renin. It also prevents diuresis byaltering receptors in the collecting ducts ofthe kidneys.

Endothelin 1, produced in endothelial vas-cular smooth muscle cells in neurons and inendometrial cells, acts as a modulator ofvasomotor tone, cell proliferation, and hor-mone production. Its release is stimulated byshear stress and the presence of angiotensinII, vasopressin, and epinephrine. And—youguessed it—it’s yet another potent vasocon-strictor; it stimulates growth of myocytes(beating heart cells) in heart failure.

Angiotensin II stimulates the adrenal

gland to secrete aldosterone, which acts toretain both sodium and water. This results incompensatory changes in the structure of theheart. Both the ventricles and the atria beginto dilate in response to the excess fluid vol-ume. According to the Frank-Starling law ofthe heart, the increased volume (increasedpreload) results in greater contractility andgreater cardiac output.

A fourth mechanism to boost low cardiacoutput is to increase the stroke volume byincreasing the amount of water in the blood-stream. Stroke volume, simply put, is theamount of blood pumped by the left ventri-cle in a single contraction.

The final compensatory mechanism is therelease of two amino acid peptides: humanatrial natriuretic peptide (hANP) and humanbrain natriuretic peptide (hBNP). hANP isreleased by stretch receptors in the atria, andhBNP is released by stretch receptors in theventricles, both in response to excess bloodvolume. Their purpose is to cause a loss ofsodium and water via the kidneys; hBNPalso provides balanced vasodilatation ofveins, arteries, and coronary arteries,which reduces the blood pressure andimproves blood flow through the coro-nary arteries. Human BNP reduces aldos-terone levels, which helps to promote sodi-um and water excretion.

When a patient is in compensated heart

Up to apoint, thebody can

compensatefor theheart’sfailings.

Helping handson the WebThe American Heart Association recommendsthe following organizations to help caregiversand individuals cope with chronic heart failure:• The Mended Hearts, Inc.:

http://www.mendedhearts.org• Heartmates:

http://www.heartmates.com• National Family Caregivers Association:

http://www.nfcacares.org• The Well Spouse Association:

http://www.wellspouse.org.


failure, all of the aforementioned mecha-nisms work together in a balanced mannerto maximize cardiac output. They act toprevent signs and symptoms of decom-pensation.

Let’s examine next what happens whenheart failure overpowers the compensatorymechanisms.

No safety netDecompensated heart failure is a loss ofbalance between the mechanisms of heartfailure and the body’s attempts to over-come the failure process. As a result, thepatient begins to show the signs andsymptoms of heart failure. Heart failurecan be left-sided, right-sided, or both.

Left-sided heart failure can be recognized bycrackles in the posterior lung fields due toexcessive preload. The patient will be tachy-cardic, dyspneic, and tachypneic. She mayhave a low SpO2 via pulse oximetry andcomplain of having to lie propped up to

sleep. She may givea history of wakingwith paroxysmalnocturnal dyspnea.Auscultation mayreveal an S3/S4gallop.

Also, low bloodflow through themesenteric arteriesmay cause symp-toms of reducedblood flow to thegastrointestinaltract, includinganorexia, nausea,bloating, and con-stipation. Lowblood flow throughthe renal arterycauses reduced uri-nary output.Vasoconstrictionfrom angiotensin IIand vasopressin

may cause cool or cold, pale, and possiblycyanotic extremities.

Right-sided heart failure is expressed as signsand symptoms caused by excessive preloadon the right side of the heart: jugular venousdistention, liver engorgement, ascites, andperipheral edema. Both left-sided and right-sided heart failure are associated with anincrease in weight.

These signs and symptoms are suggestiveof heart failure. Now let’s see how the diag-nosis is made.

Hear that?The most commonly used and useful diag-nostic test for heart failure is the transtho-racic echocardiogram. It provides the mostinformation about the structure and func-tion of the heart. Coupled with Dopplerflow studies, it can show atrial and/orventricular hypertrophy, valve problems,whether the problem is inside the heart orin the pericardium, and when the problemoccurs (during systole or diastole). Theechocardiogram can compute ejection frac-tion and determine whether any of theheart walls are failing to contract normally.

Other helpful tests include 12-lead ECG,chest X-ray, radionuclide ventriculography,and magnetic resonance imaging or comput-ed tomography. The 12-lead ECG and chestX-ray alone don’t provide adequate informa-tion to make a reliable diagnosis.

A left heart catheterization with a ven-triculogram can also provide importantinformation about the patency of the coro-nary arteries, as well as structure and func-tion of the left ventricle. The procedure isinvasive, however, requiring injection of acontrast medium into the heart. The contrastmedium is excreted through the kidneys,which can cause problems in certain patientswith impaired renal function. Some patientsmay have an adverse reaction to the contrastmedium.

A right heart catheterization is useful formeasuring the pressures in the right side ofthe heart. This test is also invasive. It’s used

Signs andsymptomschecklistLeft-sided heart failure• Crackles (posterior lung fields)• Tachycardia• Dyspnea• Tachypnea• Low SpO2• Paroxysmal noctural dyspnea• Gastrointestinal symptoms (anorexia, nau-sea, bloating, constipation)• Reduced urinary output• Cool or cold, pale, possibly cyanotic extrem-ities• Weight gainRight-sided heart failure• Jugular venous distention• Liver engorgement• Ascites• Peripheral edema• Weight gain

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mainly to evaluatethe degree of heartfailure and to guidetherapies when thepresence of moder-ate to severe heartfailure is known orsuspected.

Once heart failureis diagnosed, treat-ment begins. Let’slook at what’s avail-able.

Battling backTreatment is de-signed to restorethe balance be-tween compensa-tory and decom-pensatory mecha-nisms. Here’s the

equation again: cardiac output = stroke vol-ume x heart rate. Let’s look at the treatmentoptions for the three components of strokevolume, one at a time.• Preload—Recall that preload is theamount of fluid in the ventricles at the endof diastole. The first line of treatment forheart failure, therefore, is to reduce the pre-load, typically with a diuretic. That usuallymeans I.V. furosemide (Lasix), which pro-vides a relatively quick diuresis. It’s espe-cially useful if the patient is in respiratorydistress from left-sided heart failure.

ACE inhibitors are also used to reducepreload. They act as vasodilators, and theypromote excretion of sodium and waterthrough the kidneys.

Nesiritide (Natrecor), a synthetic BNP,mimics the actions of endogenous natri-uretic peptides. It promotes diuresis bycausing the kidneys to excrete largeamounts of sodium and water. It workswith furosemide to cause rapid diuresis todecrease preload. ■ Afterload—As the body tries to compen-sate for heart failure by raising the blood

pressure through the renin-angiotensin-aldosterone system, afterload may becometoo high. Because ACE inhibitors are vaso-dilators, they’re used to reduce both after-load and preload. Beta-blockers, nitrates,and hydralazine may also be used to pro-mote vasodilatation.

Nesiritide causes balanced arterial andvenous dilatation, thus lowering systemicblood pressure. The left ventricle is betterable to eject the blood when the blood pres-sure comes down, which increases cardiacoutput.

Nesiritide has also been shown to reduceserum levels of norepinephrine and aldos-terone, indicating that it can blunt activationof the renin-angiotensin-aldosterone systemin heart failure. Metoprolol (Lopressor), abeta-blocker, and carvedilol, a combinationof alpha- and beta-blockers, also slow activa-tion of the renin-angiotensin-aldosteronesystem.

Spironolactone (Aldactone) acts as apotassium-sparing diuretic and an aldos-terone antagonist; it reverses sodium andwater retention. Patients given spironolac-tone and an ACE inhibitor have been shownto have better ventricular function and exer-cise tolerance than those given an ACEinhibitor alone.

Eplerenone (Inspra), another aldosteroneantagonist, is used for patients who developheart failure following an MI.■ Contractility—If the heart’s contractilityis strengthened, cardiac output improves.Digoxin (Lanoxin), a digitalis glycoside, in-creases the strength of contractions andslows the heart rate. Although once the cor-nerstone of heart failure treatment, digoxinis now used less often and at lower doses.

Currently, research is under way to test animplantable device to improve cardiac con-tractility. The device delivers a small amountof electricity, similar to a pacemaker, to opencalcium channels in the heart muscle cells.The theory behind the device is that by mak-ing extra calcium available, the myofibrils willimprove the strength of their contractions.

Drug therapyfor heart failureDrugs to reduce preload• Diuretics, such as furosemide (Lasix)• Angiotensin-converting enzyme (ACE)inhibitors• Nesiritide (synthetic BNP)Drugs to reduce afterload• ACE inhibitors• Beta-blockers• Nitrates• Hydralazine• Nesiritide• Metoprolol • Carvedilol• Spironolactone• EplerenoneDrugs to improve contractility• Digoxin (not used as often as it once was)• Levosimendan (still experimental)

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Levosimendan, a calcium sensitizer, is in aPhase III clinical trial designed to study itseffects on patients with class III or IV heartfailure. Besides providing vasodilation, itimproves contractility of the heart duringsystole and allows more normal relaxationduring diastole.

Now, let’s see what your role is in caringfor patients with heart failure.

Catch your breathRemember, your first considerations in car-ing for a patient in heart failure are relatedto affecting preload adjustments. You needto begin by assessing the patient’s clinical

signs and symptoms. Mrs. Singer, you’ll re-call, came into the ED with dyspnea, tachy-cardia, and tachypnea. Auscultation re-vealed crackles in the posterior lung fieldsbilaterally and an S3 gallop. These are signsof increased left ventricular preload. Mrs.Singer also displayed neck vein distention,liver engorgement, and pedal edema,which reflect an increase in right ventricu-lar preload.

Once you take vital signs on a patient likeMrs. Singer and give her supplemental oxy-gen, you should weigh her. This baselineweight is vitally important in evaluating theeffectiveness of therapies.

The ins and outs of the heart…To better understand stroke volume, think of the heart as a balloon that’s constantly being inflated and deflated.

Preload: InflationPreload is the stretching of musclefibers in the cardiac ventricles. Itreflects the end-diastolic volume,which is influenced by diastolic pres-sure and the composition of themyocardial wall. The Frank-Starlingprinciple states that the degree of pre-load within a physiologic range is pro-portional to the systolic performance ofthe ensuing ventricular contraction.Because ventricular function is abnor-mal in heart failure, the response isinadequate.

Contractility: It’s a stretchContractility refers to the inherent abili-ty of the myocardium to contract nor-mally. It’s influenced by preload: thegreater the preload, the more forcefulthe contraction of the heart muscle.Contractility is characterized by theforce and velocity of contraction; it’soften expressed as the ejection fraction(left ventricular stroke volume/end-diastolic volume).

Afterload: DeflationAfterload refers to the pressure that theventricular muscles need to exert toovercome the higher pressure in theaorta to move blood out of the heart.Resistance is the force the heart mus-cle must counteract. Afterload is deter-mined by ventricular pressure, bloodvolume in the chamber, and wall thick-ness at the time of the aortic valveopening.


Remindyour patientto lose hersalt shaker

when shegets home!

Medical therapies that are implementedearly on may include an I.V. bolus dose of adiuretic, followed perhaps by a continuousinfusion of diuretics, along with administra-tion of an ACE inhibitor and/or a beta-blocker, as prescribed.

Position the patient for comfort. Gener-ally, the semi-Fowler’s position or seated onthe edge of the bed with her arms resting onthe over-bed table works well. Advise thepatient that her daily fluid intake is limitedto 1 to 2 liters. If she has a dry mouth, shecan relieve it by brushing her teeth and rins-ing her mouth with water or mouthwash.Also, tell her that it’ll be important for hernurses to keep accurate records of intake andoutput to evaluate the success of her thera-py. During her hospital stay, she’ll likely be

put on a 2 g/day sodium diet andgiven recommendations for dietary

restrictions after discharge.Next, we’ll look at interventions relat-

ed to the effect of increased afterload.

Take a load offTo increase cardiac output in heart fail-

ure, afterload needs to be lowered to im-prove stroke volume of the impaired leftventricle. Remember, afterload is theamount of resistance the heart has to over-come to eject blood from the ventricle. It’sinfluenced by the volume and mass ofblood ejected, the size and wall thicknessof the ventricle, and the impedance of thevasculature.

Administration of vasodilators (nesiritide,ACE inhibitors, beta-blockers, or hydralazineplus nitrates) is effective, and doses can beadjusted according to the measurementsfrom the right heart catheter. How can youtell if the drug therapy is succeeding? Here’sone indicator: pulse pressure, the differencebetween systolic and diastolic blood pres-sures. The narrower the pulse pressure, thegreater the afterload. A widening pulse pres-sure is associated with a decrease in after-load.

Whether you use pulse pressure or not,

it’s important to monitor blood pressureclosely with these drugs. The best bloodpressure is one that’s as low as the patientcan tolerate without getting dizzy. Continuegiving the vasodilator, even if the systolicpressure is only in the 90s. Withholding thevasodilator will just allow the afterload toincrease, causing cardiac output to fall. If thesystolic pressure falls below 90 and thepatient becomes dizzy, however, therapymay need to be adjusted. In the case of nesir-itide, for example, the infusion should bestopped until the systolic pressure rises over90. Then, the infusion can be resumed at 30%of the previous rate; no bolus is given whenthe infusion is resumed.

Mrs. Singer’s progressTo evaluate the effect of her therapy, Mrs.Singer’s nurse in the cardiac care unit(CCU) takes her vital signs again and doesanother physical assessment. Mrs. Singer’sheart rate is now below 100 and her respi-ratory rate is at 22. Within about 3 hoursof being treated with I.V. furosemide inthe ED, Mrs. Singer states that she’s lessshort of breath. She also received a bolusand infusion of nesiritide in the ED beforebeing transferred to the CCU. Her bloodpressure is now 98/56; she denies feelingdizzy. Her diastolic pressure indicates thewonderful afterload reduction achieved bythe combination of therapies.

The crackles in Mrs. Singer’s lung fieldshave decreased to fine bibasilar crackles.During the next couple of days, her jugularvenous distention and edema are reduced.She’s producing more urine than liquidtaken by mouth, and her daily weights con-firm this: Her 24-hour intake and outputlevel is 2 L negative, and she’s 4.4 poundslighter.

Now that Mrs. Singer’s feeling better, it’stime to start teaching her about better man-agement of heart failure. Patient teachingshould include medications, fluid manage-ment, low-sodium diet, daily weights, andthe importance of regular exercise. A patient


who smokes should be advised to stop. Mrs.Singer should also be told to avoid usingnonsteroidal anti-inflammatory drugs forpain because they may cause sodium reten-tion and myocardial depression. Takingmedications as prescribed and followingstrict fluid-management and sodium-reduction plans after discharge will greatlyreduce the number of rehospitalizations forrecurrence of symptoms.

Stress the importance of notifying the pri-mary health provider or cardiologist imme-diately after a gain of 2 pounds overnight or5 pounds in a week, or after awakening sud-denly with shortness of breath.

Smooth sailingHeart failure is a major and growinghealth care issue due to an aging popula-tion, improved survival after an MI, andimprovements in the management ofchronic heart failure. Nursing care is vi-tally important in all health care settings.It’s our job as nurses to evaluate our pa-tients’ responses to all therapies. A good

understanding of preload and afterloadcan help you to make the best clinical de-cisions when managing your patients withheart failure.

Because of the prompt and effectivetreatment Mrs. Singer received, she andHarry will be able to go on that Caribbeancruise they’ve been looking forward to forso long! ■

Learn more about itAdams KL. Hemodynamic assessment: The physiologicbasis for turning data into clinical information. AACNClinical Issues: Advanced Practice in Acute and Critical Care.15(4):534-546, October/December 2004.

Heart Failure Society of America. Patient education mod-ules. http://www.abouthf.org/education_modules.htm.Accessed November 2, 2005.

Hunt SA, et al. ACC/AHA 2005 Guideline Update for theDiagnosis and Management of Chronic Heart Failure inthe Adult—Summary Article. A Report of the AmericanCollege of Cardiology/American Heart Association TaskForce on Practice Guidelines (Writing Committee to Up-date the 2001 Guidelines for the Evaluation and Manage-ment of Heart Failure). Journal of the American College ofCardiology. 46(6):1116-1143, September 2005.

Morrison L, et al. Utility of a rapid B-natriuretic peptideassay in differentiating congestive heart failure from lungdisease in patients presenting with dyspnea. Journal of theAmerican College of Cardiology. 39(2):202-209, June 2002.

INSTRUCTIONS

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PROVIDER ACCREDITATION:This Continuing Nursing Education (CNE) activity for 2.5 contacthours is provided by Lippincott Williams & Wilkins (LWW), which isaccredited as a provider of continuing education in nursing by theAmerican Nurses Credentialing Center’s Commission onAccreditation and by the American Association of Critical-Care Nurses(AACN 00012278, CERP Category A). This activity is also providerapproved by the California Board of Registered Nursing, ProviderNumber CEP 11749 for 2.5 contact hours. LWW is also an approvedprovider of CNE in Alabama, Florida, and Iowa, and holds the follow-ing provider numbers: AL #ABNP0114, FL #FBN2454, IA #75. All ofits home study activities are classified for Texas nursing continuingeducation requirements as Type 1. Your certificate is valid in allstates. This means that your certificate of earned contact hours isvalid no matter where you live.

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take note!Remember that iceor anything frozenmust be counted asa liquid. Usually, thevolume of ice is esti-mated to be equalto half that of liquidvolume.


1. Which of the following are considered the cardinal signsof heart failure?a. shortness of breath, hypotension, and edemab. anxiety, chest pain, and diaphoresisc. dyspnea, fatigue, and fluid retention

2. Which of the following best describes what happens tothe body in heart failure?a. The heart can’t supply sufficient quantities of blood and

oxygen to meet the metabolic needs of the body’s tissues.b. The lungs can’t sufficiently oxygenate the blood, resulting in

a decreased workload to the heart.c. The heart muscle relaxes, resulting in an enlarged heart and

improved pumping ability.

3. Which of the following is true about remodeling?a. It happens quickly. b. It results in dilation of the atria only.c. It begins with some type of injury to the myocardium.

4. Hyperthyroidism and anemia can cause a. low-output heart failureb. high-output heart failurec. biventricular failure

5. Normal ejection fraction isa. 40% to 55%.b. 60% to 80%.c. 85% to 95%.

6. Long-standing systemic hypertension can lead toa. left ventricular diastolic dysfunction.b. right ventricular systolic dysfunction.c. idiopathic dilated cardiomyopathy.

7. A patient experiences fatigue, palpitations, and dyspneawith normal activity. Which NYHA functional class wouldbe assigned? a. Class IIb. Class IIIc. Class IV

8. Raising the heart rate causes the cardiac output toa. also increase.b. decrease.c. stay the same.

9. Which of the following is a compensatory mechanism tomaximize the functioning of the heart?a. reduction of the stroke volume by decreasing the amount of

water in the bloodstreamb. stimulation of the parasympathetic nervous systemc. activation of the renin-angiotensin-aldosterone system

10. A patient with only jugular venous distention and pe-

ripheral edema most likely has which type of heart failure?a. left-sided heart failureb. right-sided heart failurec. biventricular heart failure

11. Which of the following is the most commonly used andmost useful diagnostic test for heart failure? a. 12-lead electrocardiogramb. cardiac catheterization with ventriculogramc. transthoracic echocardiogram

12. The amount of fluid filling the ventricles at the end ofdiastole is calleda. preload.b. afterload.c. stroke volume.

13. The first-line treatment for heart failure is to reducea. preload.b. afterload.c. contractility.

14. Which of the following drugs is usually the initial treat-ment of heart failure?a. digoxin (Lanoxin)b. furosemide (Lasix)c. metoprolol (Lopressor)

15. Obtaining a baseline weight for a patient with heartfailure is most important fora. assessing intake and output. b. indicating when the patient

needs to have afterload in-creased.

c. evaluating the effectiveness oftherapies.

16. Administration of nesiri-tide results ina. fluid retention.b. an increase in preload.c. a decrease in preload.

17. Advise your patient to notify her primary careprovider or cardiologist ifshea. awakens at night to

urinate.b. loses 5 pounds in

a week. c. gains 2 pounds

overnight.

Too pooped to pump: Managing chronic heart failureGENERAL PURPOSE: To familiarize the registered professional nurse with the pathophysiology of heart failure and appropriatetreatment and nursing care for the patient. LEARNING OBJECTIVES: After reading the article and taking this test, you shouldbe able to: 1. Describe the pathophysiology and signs and symptoms of heart failure. 2. Discuss the diagnosis and treatment ofheart failure.

2.5 ANCC/AACN CONTACT HOURS

Turn to page 52 for the CE Enrollment Form.

Ready? Failureisn’t an option!

Date post:	18-Nov-2014
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Too Pooped to Pump

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