learning objectives - weeblynursing4all.weebly.com/uploads/9/5/4/8/9548528/ch30.pdfally managed in...

Management of PatientsWith Complications FromHeart Disease

On completion of this chapter, the learner will be able to:1. Describe the management of patients with chronic heart failure.2. Use the nursing process as a framework for care of patients with

heart failure.3. Describe the management of patients with acute heart failure.4. Develop teaching plans for patients with heart failure.5. Describe the management of patients with cardiogenic shock.6. Describe the management of patients with thromboembolic

episodes, pericardial effusion and cardiac tamponade, and myocardial rupture.

7. Demonstrate the techniques of cardiopulmonary resuscitation.

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LEARNING OBJECTIVES ●

788 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION

cle during diastole. Another factor that determines preload is ven-tricular compliance, which is the elasticity or amount of “give”when blood enters the ventricle. Elasticity is decreased when themuscle thickens, as in hypertrophic cardiomyopathy (see Chap. 29)or when there is increased fibrotic tissue within the ventricle.Fibrotic tissue replaces dead cells, such as after a myocardial in-farction (see Chap. 28). Fibrotic tissue has little compliance,making the ventricle stiff. Given the same volume of blood, anoncompliant ventricle has a higher intraventricular pressurethan a compliant one. The higher pressure increases the work-load of the heart and can lead to heart failure (HF).

Afterload refers to the amount of resistance to the ejection ofblood from the ventricle. To eject blood, the ventricle must over-come this resistance. Afterload is inversely related to SV. The majorfactors that determine afterload are the diameter and distensibilityof the great vessels (aorta and pulmonary artery) and the openingand competence of the semilunar valves (pulmonic and aorticvalves). The more open the valves, the lower the resistance. If thepatient has significant vasoconstriction, hypertension, or a narrowedopening from a stenotic valve, resistance (afterload) increases. Whenafterload increases, the workload of the heart must increase to over-come the resistance and eject blood.

Contractility, which refers to the force of contraction, is re-lated to the number and status of myocardial cells. Cate-cholamines, released by sympathetic stimulation such as exerciseor from administration of positive inotropic medications, can in-crease contractility and stroke volume. MI causes necrosis ofsome myocardial cells, shifting the workload to the remainingcells. Significant loss of myocardial cells can decrease contractil-ity and cause HF. Afterload must be reduced by stress reductiontechniques or medications to match the lower contractility.

Today, the patient with heart disease can be assisted to livelonger and achieve a higher quality life than even a decade ago.Through advancements in diagnostic procedures that allowearlier and more accurate diagnoses, treatment can begin well be-fore significant debilitation occurs. Newer treatments, technologies,and pharmacotherapies are being developed rapidly. However,heart disease remains a chronic condition, and complications maydevelop. This chapter presents the complications most often re-sulting from heart diseases and the treatments provided by thehealth care team for these complications.

Cardiac HemodynamicsThe basic function of the heart is to pump blood. The heart’sability to pump is measured by cardiac output (CO), the amountof blood pumped in 1 minute. CO is determined by measuringthe heart rate (HR) and multiplying it by the stroke volume (SV),which is the amount of blood pumped out of the ventricle witheach contraction. CO usually is calculated using the equationCO = HR × SV.

One of the factors controlling HR is the autonomic nervoussystem. When SV falls, the nervous system is stimulated to in-crease HR and thereby maintain adequate CO. SV depends onthree factors: preload, afterload, and contractility.

Preload is the amount of myocardial stretch just before sys-tole caused by the pressure created by the volume of blood withinthe ventricle. Like a rubber band, the ventricular muscle fibersneed to be stretched (by the blood) to produce optimal ejectionof blood. Too little or too much muscle fiber stretch decreases thevolume of blood ejected. The major factor that determines pre-load is venous return, the volume of blood that enters the ventri-

Glossaryafterload: the amount of resistance to ejec-

tion of blood from a ventricleanuria: urine output of less than 50 mL

per 24 hourscardiac failure: heart failurecardiac output (CO): the amount of blood

pumped out of the heart in 1 minutecompliance: the elasticity or amount of

“give” when blood enters the ventriclecongestive heart failure (CHF): a fluid

overload condition (congestion) that mayor may not be caused by HF; often anacute presentation of HF with increasedamount of fluid in the blood vessels

contractility: the force of ventricular con-traction; related to the number and stateof myocardial cells

diastolic heart failure: the inability of theheart to pump sufficiently because of analteration in the ability of the heart to fill;current term used to describe a type of HF

dyspnea on exertion (DOE): shortness ofbreath that occurs with exertion

ejection fraction (EF): percent of bloodvolume in the ventricles at the end of diastole that is ejected during systole; ameasurement of contractility

heart failure (HF): the inability of the heartto pump sufficient blood to meet the needs

of the tissues for oxygen and nutrients;signs and symptoms of pulmonary andsystemic congestion may or may not bepresent

left-sided heart failure (left ventricular failure): inability of the left ventricle to fillor pump (empty) sufficient blood to meetthe needs of the tissues for oxygen and nutrients; traditional term used to describepatient’s HF symptoms

oliguria: diminished urine output; less than400 mL per 24 hours

orthopnea: shortness of breath when lying flatparoxysmal nocturnal dyspnea (PND):

shortness of breath that occurs suddenlyduring sleep

pericardiocentesis: procedure that involvessurgically opening the pericardial sac

pericardiotomy: surgically created openingof the pericardium

preload: the amount of myocardial stretchjust before systole caused by the pressurecreated by the volume of blood within aventricle

pulmonary edema: abnormal accumulationof fluid occurring in the interstitial spacesor in the alveoli of the lungs

pulseless electrical activity (PEA): condi-tion in which electrical activity is present

but there is not an adequate pulse orblood pressure because of ineffective cardiac contraction or circulating bloodvolume

pulsus paradoxus: systolic blood pressurethat is more than 10 mm Hg higher during exhalation than during inspira-tion; difference is normally less than 10 mm Hg

right-sided heart failure (right ventricularfailure): inability of the right ventricle to fill or pump (empty) sufficient blood tothe pulmonary circulation

stroke volume (SV): amount of bloodpumped out of the ventricle with eachcontraction

systolic heart failure: inability of the heart to pump sufficiently because of analteration in the ability of the heart tocontract; current term used to describe atype of HF

thermodilution: method of determiningcardiac output that involves injecting fluidinto the pulmonary artery catheter. A ther-mistor measures the difference between thetemperature of the fluid and the tempera-ture of the blood ejected from the ventricle.Cardiac output is calculated from thechange in temperature.

Chapter 30 Management of Patients With Complications From Heart Disease 789

NONINVASIVE ASSESSMENT OF CARDIAC HEMODYNAMICSSeveral noninvasive assessment findings can indicate cardiac he-modynamic status, although the findings do not directly correlateto preload, afterload, or contractility. Right ventricular preloadmay be estimated by measuring jugular venous distention. Elevatedleft ventricular preload may be identified by a positive hepatojugu-lar test. Mean arterial blood pressure is a rough indicator of left ven-tricular afterload. Activity tolerance may be used as an indicator ofoverall cardiac functioning. These assessments are described inmore detail later in the chapter.

Impedance cardiography (ICG) is a noninvasive method forcontinuous calculation of SV, CO, systemic vascular resistance,ventricular contractility, and fluid status (Turner, 2000). Elec-trodes are placed on the patient’s chest. The electrodes are con-nected to a device that transmits a very small amount of alternatingelectric current through the chest and measures the resistance (Z)to the flow (conduction) of the current. Because the current seeksthe path of least resistance and fluid is an excellent conductor, thecurrent flows through the blood. ICG measures the volume ofblood flow.

The cardiac cycle produces normal changes in blood flow vol-ume; for example, there is more blood flow volume during systoleand less blood flow volume during diastole. The changes in bloodflow volume change the resistance to flow of the current, which iscalled electrical impedance (dZ). During systole, the higher bloodflow volume causes the red blood cells to be aligned in a more par-allel pattern, which makes the flow of current faster and reducesimpedance. During diastole, the lower blood flow volume causesthe red blood cells to be more randomly arranged, which makesthe flow of current slower and increases impedance. Stroke vol-ume is determined by comparing dZ to the changes in time (dt)(Von Rueden & Turner, 1999). The preejection period (PEP) andventricular ejection times (VET) can be measured, which furtherassists in understanding the hemodynamic status of the patient.For example, a dysfunctional left ventricle requires more time togenerate pressure to overcome the resistance to ejection so that theaortic valve opens (increased PEP) and has less time during whichblood is ejected into the aorta (decreased VET).

INVASIVE ASSESSMENT OF CARDIAC HEMODYNAMICSAn important method for evaluating the components of SV in ahemodynamically unstable patient is the pulmonary artery (PA)catheter, which is used to obtain the hemodynamic data essentialfor diagnosis and treatment (see Chap. 26). Connected to a com-puterized transducer apparatus, the PA catheter serves as a fluid-filled conduit for detecting pressure changes within the heart.The pulsatile changes in pressure are converted into electrical sig-nals, which are displayed as waveforms on a monitor (Fig. 30-1;Chart 30-1).

CO is measured most often by the thermodilution methodwith the thermistor port of the catheter. The port is connected toa computer that calculates CO and other cardiac parameters. Inthermodilution, a specific volume of fluid that is colder than thepatient’s blood is injected into the proximal port (right atrium).The fluid enters the right ventricle and is then ejected into thePA. The thermistor records the temperature before and after theejection of fluid. The change in temperature is inversely relatedto CO; the greater the CO, the faster the blood and fluid moves,the less time the fluid has to mix with the blood to cause a change

in temperature, and the less change in temperature detected bythe thermistor.

Cardiac parameters for afterload and contractility are calcu-lated at the same time as CO (Table 30-1). Measurements of thevarious pressures are made at intervals. Therapy, especially intra-venous medication, is adjusted based on the assessment and di-agnostic findings.

The patient with an invasive hemodynamic catheter is usu-ally managed in an intensive care environment (see Chart 30-1)because of the need for frequent nursing assessments and inter-ventions.

Heart FailureHF, often referred to as congestive heart failure (CHF), is theinability of the heart to pump sufficient blood to meet the needsof the tissues for oxygen and nutrients. However, the term CHFis misleading, because it indicates that patients must experiencepulmonary or peripheral congestion to have HF, and it impliesthat patients with congestion have HF. The Agency for HealthCare Policy and Research (AHCPR) HF guidelines panel (1994)defined HF as a clinical syndrome characterized by signs andsymptoms of fluid overload or of inadequate tissue perfusion.These signs and symptoms result when the heart is unable to gen-erate a CO sufficient to meet the body’s demands. The HF guide-line panel used the term heart failure because many patients withHF do not manifest pulmonary or systemic congestion. Theterm HF is preferred and indicates myocardial heart disease inwhich there is a problem with contraction of the heart (systolicdysfunction) or filling of the heart (diastolic dysfunction) andwhich may or may not cause pulmonary or systemic congestion.Some cases of HF are reversible, depending on the cause. Mostoften, HF is a life-long diagnosis that is managed with lifestylechanges and medications to prevent acute congestive episodes.CHF is usually an acute presentation of HF.

CHRONIC HEART FAILUREAs with coronary artery disease, the incidence of HF increases withage. However, the rate of coronary artery disease is decreasing andjust the opposite is true for HF. Nearly 5 million people in theUnited States have HF, with more than one-half million new casesdiagnosed each year (American Heart Association, 2001). Theprevalence rate of HF among non-Hispanic whites 20 years of ageor older is 2.3% for men and 1.5% for women; for non-Hispanicblacks, the rates are 3.5% and 3.1%, respectively (American HeartAssociation, 2001). HF is the most common reason for hospital-ization of people older than age 65 and the second most commonreason for visits to a physician’s office. The rate of readmission tothe hospital remains staggeringly high. The rise in the incidenceof HF reflects the increased number of elderly and improvementsin treatment of HF resulting in increased survival rates. However,the economic burden caused by HF is estimated to be more than23 billion dollars in direct and indirect costs and is expected to in-crease (American Heart Association, 2001). Many hospitalizationscould be prevented by improved and appropriate outpatient care.Prevention and early intervention to arrest the progression of HFare major health initiatives in the United States.

Medical management is based on the type, severity, and cause ofHF. There are two types of HF, which are identified by assessmentof left ventricular functioning: an alteration in ventricular filling(diastolic heart failure) and an alteration in ventricular contraction

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Pressure bag

Superiorvena cava

Pulmonaryartery

Ballooninflationvalve(port)

Cables

IV tubing

Distallumen

Proximallumen

Distal lumen opening

Ballooninflated

Cross sectionTransducer/flush devices

Proximal (RA)infusion port

Distal (PA)infusion port

Normal salineIV solution(flush)

Multilumenpulmonaryarterycatheter

Ballooninflationlumen

Thermistorlumen

Distal(PA) lumen

Proximal(RA) lumen

Thermistorlumen opening

EKG

PA

RA

Monitor

Pressuretubings

Thermistorconnector

FIGURE 30-1 The pulmonary artery (PA) catheter system serves as a fluid-filled conduit for detecting pressurechanges within the heart. (A) The PA catheter is inserted through a sheath into the superior vena cava, usually via the rightinternal jugular or subclavian vein. It is connected to pressure tubing (B) which is then connected to a transducer (C). Thetransducer detects pulsatile changes in pressure and converts them into electrical signals. These signals are convertedinto waveforms, which are shown on a monitor (D). The transducer also contains a flush device (E) that automaticallyinfuses a small amount of flush fluid through the catheter to help maintain its patency. Because of the pressure that theheart generates, pressure is applied to the flush fluid to ensure that the fluid flows into the catheter and into the blood-stream and that blood does not flow back into the catheter. The PA catheter contains several lumens (F) with openingslocated at various intervals. These lumens allow for the measurement of hemodynamic pressures at different points. Theproximal port is usually in the right atrium and is used to measure central venous pressure (CVP). The distal tip of thecatheter rests in the pulmonary artery and measures the pulmonary artery systolic and diastolic pressures. When the bal-loon is inflated (G), the tip floats into smaller branches of the pulmonary artery until it can no longer pass, that is, untilit is “wedged” in the vessel. The distal tip then records the pressure in front of it, called pulmonary artery wedge pres-sure (PAWP). Cardiac output is measured most often by the thermodilution method with the thermistor port. The portis connected to a computer that calculates cardiac output and other cardiac parameters.


ACTIONS RATIONALE/AMPLIFICATION

1. The information may assist in reducing the patient’s anxiety,which may also help to limit the patient’s movement during theprocedure.

2. An initial assessment provides a baseline for comparison.3. The patient is usually placed in a flat or Trendelenburg

position to minimize the risk of air embolization and facilitateaccess.

4. Monitoring systems and setups vary according to manufacturer.a. The complexity of the setup requires an understanding of the

equipment in use.

b. Flushing the catheter system ensures patency and eliminates airbubbles.

c. Testing for leakage ensures that the balloon is intact.5. Decreases risk of infection at insertion site

1. The internal jugular vein insertion site has standard landmarks,establishes a straight route into the central venous system, and isassociated with few complications. The subclavian insertion siteallows the patient more mobility. It is also easier to secure thecatheter from this site.

2. Catheter placement is determined by characteristic waveformsand changes.

3. The amount of air to be used is indicated on the catheter.

4. Watching the ECG monitor for signs of ventricular irritability asthe catheter enters the right ventricle allows dysrhythmias to bereported to the physician promptly. Subsequent pressure readingsare taken from this baseline.

5. With the catheter in the wedge position, the balloon blocks theflow of blood from the right side of the heart toward the lungs.The resulting artery wedge pressure (PAWP) correlates with themean left ventricular end-diastolic pressure.

6. Wedge pressure is a valuable measure of cardiac function. Lower-than-normal pressure readings indicate hypovolemia. Higher-than-normal pressure readings indicate hypervolemia and/or leftventricular failure.

7. The normal pulmonary artery systolic pressure is 15 to 30 mmHg, and the diastolic pressure range is 10 to 15 mm Hg. Thenormal mean pulmonary artery pressure (average pressure in pul-monary artery throughout the entire cardiac cycle) ranges from10 to 20 mm Hg. Elevated pulmonary pressures can indicate several clinical problems, such as pulmonary disease, mitral valvedisease, and ventricular failure.

Preparatory Phase1. Explain the procedure to the patient, family, and significant others.

2. Check vital signs and apply ECG electrodes.3. Position the patient to allow the physician access to the insertion

site, decrease the risk of complications, and promote patient com-fort. To ensure consistency, the angle of elevation should be doc-umented if the patient cannot lie flat.

4. Set up equipment according to manufacturer’s directions.a. The pulmonary artery (PA) catheter requires pressure tubing, a

transducer, a flush system, and a pressure amplifier connectedto a monitoring–recording system. In addition, an IV pole anda transducer holder are usually needed.

b. The pressure equipment is calibrated and flushed according tothe manufacturer’s directions.

c. The balloon is inflated with air to test for leakage.5. Prepare the skin over the insertion site.

Performance Phase (Physician Responsibility)1. The PA catheter is inserted through a sheath that has been placed

in the internal jugular, subclavian, or any easily accessible, large-diameter vein by percutaneous puncture or venotomy. Thesheath may be surrounded by a protective cover that maintainsthe sterility of the catheter.

2. The catheter is advanced while observing the monitor for pressurewaveforms, which indicate the placement of the tip of thecatheter within the heart. Occasionally fluoroscopy is used to ver-ify proper placement of the PA catheter.

3. When the catheter is in the large vein, the balloon is inflated to itsrecommended volume.

4. The patient’s blood flow will gently pull the inflated balloon atthe tip of the catheter through the right atrium and tricuspidvalve into the right ventricle and into the main pulmonaryartery. The monitoring equipment displays specific pressurewaveforms as the catheter advances through the various cham-bers of the heart. These initial waveforms and pressures arerecorded.

5. The flowing blood will continue to direct the catheters more distallyinto the pulmonary arteries. When the catheter reaches a pulmonaryvessel that is approximately the same size or slightly smaller indiameter than the inflated balloon, it will not advance any further.This is the wedge position from which pulmonary artery wedgepressure (PAWP) [pulmonary artery obstructive pressure (PAOP) or pulmonary capillary wedge pressure (PCWP)] is measured.

6. The pressure is recorded with the balloon wedged in the pul-monary vascular bed. A mean capillary wedge pressure between8 and 12 mm Hg indicates normal left ventricular function.

7. The balloon is then deflated, causing the catheter to retractspontaneously into a larger pulmonary artery. The change in thecatheter tip position causes a reappearance of the pulmonaryartery waveform. The pulmonary artery systolic, diastolic, andmean pressures are recorded.

Chart 30-1

GUIDELINES FOR Hemodynamic Monitoring: Multilumen Pulmonary Artery Catheter

(continued)


(systolic heart failure). An assessment of the ejection fraction(EF) is performed to assist in determining the type of HF. EF is thepercentage of the end-diastolic blood volume in the ventricleminus the end-systolic blood volume in the ventricle divided bythe end-diastolic blood volume in the ventricle—an indication ofthe amount of blood that was ejected and the contractile ability ofthe ventricle. The EF is normal in diastolic HF, whereas the EF isless than 40% in systolic HF. The severity of HF is frequently clas-sified according to the patient’s symptoms. The New York HeartAssociation classification is described in Table 30-2, and the causesare explained in subsequent sections of this chapter.

Pathophysiology

HF results from a variety of cardiovascular diseases but leads to some common heart abnormalities that result in decreasedcontraction (systole), decreased filling (diastole), or both. Signifi-cant myocardial dysfunction most often occurs before the patientexperiences signs and symptoms of HF.

Systolic HF decreases the amount of blood ejected from theventricle, which stimulates the sympathetic nervous system to re-lease epinephrine and norepinephrine. The purpose of this initialresponse is to support the failing myocardium, but the continued

ACTIONS RATIONALE/AMPLIFICATION

8. Maintaining catheter sterility in this manner allows for the ad-vancement and repositioning of the catheter if needed. Applysterile dressing.

9. Accurate position will assure accurate readings and preventcomplications.

1. Do not allow the catheter to remain in the wedge position. Thedecrease in blood flow through the pulmonary artery that occurswhen wedging the catheter may cause segmental pulmonary infarction.

2. These are standard safety measures.

1. Careful monitoring helps prevent complications. A foreign body(catheter) in the vascular system increases the risk of sepsis.

2. Ischemia may occur from inadequate arterial flow.

3. Absence of a pulse may indicate occlusion of the vessel.4. These are standard nursing practices.

1. An informed patient is less fearful; a deflated balloon is less likely toinjure the patient’s heart or blood vessels during catheter removal.

2. The supine position results in the least patient movement and isthe best position for maintaining blood pressure and venous return.

3. This prevents fluid from infusing into tissues as the catheter is removed; it also prevents air from entering the catheter.

4. Positive intrathoracic pressure minimizes the chance of air enter-ing the chest and vasculature through or around the catheter.Continuous gentle traction minimizes the risk of the catheter be-coming kinked, knotted, or tangled. A sterile dressing minimizesthe risk of infection from the skin wound.

8. The protective cover is attached to the introducer and secured tothe catheter. The catheter is sutured in place and a dry dressingplaced over the insertion site.

9. A chest x-ray to confirm catheter position and to serve as a base-line for future reference is obtained after catheter insertion.

To Obtain a Wedge Pressure Reading1. Inflate the balloon slowly until the pulmonary artery pressure

waveform changes (indicating a wedge pressure waveform) and anincrease in resistance to injection is detected. Once these changesoccur, no more air is introduced. (The amount of air to causethese changes should be less than 1.5 mL.) Most cardiac monitorsallow for freezing the wedge pressure waveform and its immediateprinting.

2. As soon as the wedge pressure is obtained, allow passive deflationof the balloon by releasing pressure on the syringe.

To make sure that the syringe cannot be inflated accidentally,remove it, push the plunger to the bottom of the barrel so that itis totally empty of air, reattach it to the PA catheter, and lock itclosed.

Follow-up Phase1. Inspect the insertion site daily. Observe for signs of infection,

swelling, and bleeding.2. In accord with protocol, record date and time of dressing change

and IV tubing change. If a peripheral vessel access site is used, assessthe extremity for color, temperature, capillary filling, and sensation.

3. Evaluate pulse.4. Assess for complications: pneumothorax, pulmonary ischemia or

infarction (due to persistent balloon wedging from inflation orcatheter migration), pulmonary artery rupture (due to overinfla-tion of the balloon), dysrhythmias, heart block, damage to tricus-pid valve, knotting of catheter within the heart or blood vessels,thromboembolus, infection, balloon rupture, hematoma at inser-tion site, and bleeding.

For Removal of the Catheter1. Explain the procedure to the patient, and make sure the balloon

is not inflated.2. Place the patient in a supine position.

3. Stop all IVs running through the PA catheter and turn stop-cocks off.

4. While the patient holds the breath or exhales, the catheter iswithdrawn gently and continuously, without excessive force ortraction; a sterile dressing is applied over the site.

Chart 30-1

GUIDELINES FOR Hemodynamic Monitoring: Multilumen Pulmonary Artery Catheter (Continued)


response causes loss of beta1-adrenergic receptor sites (down-regulation) and further damage to the heart muscle cells. Thesympathetic stimulation and the decrease in renal perfusion bythe failing heart cause the release of renin by the kidney. Reninpromotes the formation of angiotensin I, a benign, inactive sub-stance. Angiotensin-converting enzyme (ACE) in the lumen ofblood vessels converts angiotensin I to angiotensin II, a vaso-constrictor that also causes the release of aldosterone. Aldo-sterone promotes sodium and fluid retention and stimulates thethirst center. Aldosterone causes additional detrimental effectsto the myocardium and exacerbates myocardial fibrosis (Pitt et al., 1999; Weber, 2001). Angiotensin, aldosterone, and otherneurohormones (eg, atrial natriuretic factor, endothelin, andprostacyclin) lead to an increase in preload and afterload, whichincreases stress on the ventricular wall, causing an increase inthe workload of the heart.

As the heart’s workload increases, contractility of the myofi-brils decreases. Decreased contractility results in an increase inend-diastolic blood volume in the ventricle, stretching the myo-fibers and increasing the size of the ventricle (ventricular dilation).The increased size of the ventricle further increases the stress onthe ventricular wall, adding to the workload of the heart. Oneway the heart compensates for the increased workload is to in-crease the thickness of the heart muscle (ventricular hypertrophy).However, the hypertrophy is not accompanied by an adequate in-crease in capillary blood supply, resulting in myocardial ischemia.The sympathetic-induced coronary artery vasoconstriction, in-creased ventricular wall stress, and decreased mitochondrial en-ergy production also lead to myocardial ischemia. Eventually, themyocardial ischemia causes myofibril death, even in patients with-out coronary artery disease. The compensatory mechanisms of HFhave been called the “vicious cycle of HF” because the heart doesnot pump sufficient blood to the body, which causes the body tostimulate the heart to work harder; the heart is unable to respondand failure becomes worse.

Diastolic HF develops because of continued increased work-load on the heart, which responds by increasing the number andsize of myocardial cells (ie, ventricular hypertrophy and alteredmyocellular functioning). These responses cause resistance toventricular filling, which increases ventricular filling pressures de-spite a normal or reduced blood volume. Less blood in the ven-tricles causes decreased CO. The low CO and high ventricularfilling pressures cause the same neurohormonal responses asdescribed for systolic HF.

EtiologyMyocardial dysfunction is most often caused by coronary arterydisease, cardiomyopathy, hypertension, or valvular disorders. Ath-erosclerosis of the coronary arteries is the primary cause of HF.Coronary artery disease is found in more than 60% of the patientswith HF (Braunwald et al., 2001). Ischemia causes myocardialdysfunction because of resulting hypoxia and acidosis from the ac-cumulation of lactic acid. Myocardial infarction causes focal heartmuscle necrosis, the death of heart muscle cells, and a loss of con-tractility; the extent of the infarction correlates with the severity ofHF. Revascularization of the coronary artery by a percutaneouscoronary intervention or by coronary artery bypass surgery maycorrect the underlying cause so that HF is resolved.

Table 30-1 • Hemodynamic Parameters

PARAMETER RIGHT VENTRICLE LEFT VENTRICLE

PreloadNormal Values

AfterloadNormal Values

Calculation

ContractilityNormal Values

Calculation

CVP: 0–8 mm Hg

PVR: 20–120 dyne/sec/cm−5

Right ventricular stroke work index: 7–12 g/beat/m2

PAWP: 4–12 mm Hg

SVR: 800–1500 dyne/sec/cm−5

Left ventricular stroke work index: 35–85 g/beat/m2

BP, blood pressure; CO, cardiac output; CVP, central venous pressure; PA, pulmonary artery; PAP, pulmonary artery pressure; PAWP, pul-monary artery wedge pressure; PVR, pulmonary vascular resistance; SV, stroke volume; SVR, systemic vascular resistance.

mean PAP PAWP

CO80

− × Mean arterial pressure CVP

CO80

− ×

PA systolic pressure CVP SV 0.0136

Body Surface Area height and weight

−( ) × ×( )

Systolic BP PAWP SV 0.0136

Body Surface Area height and weight

−( ) × ×( )

Table 30-2 • New York Heart Association (NYHA) Classification of Heart Failure

CLASSIFICATION SYMPTOMS PROGNOSIS

I

II

III

IV

Ordinary physical activity does notcause undue fatigue, dyspnea,palpitations, or chest pain

No pulmonary congestion or peripheral hypotension

Patient is considered asymptomaticUsually no limitations of activities

of daily living (ADLs)

Slight limitation on ADLsPatient reports no symptoms at rest

but increased physical activity willcause symptoms

Basilar crackles and S3 murmur maybe detected

Marked limitation on ADLPatient feels comfortable at rest

but less than ordinary activitywill cause symptoms

Symptoms of cardiac insufficiencyat rest

Good

Good

Fair

Poor


Cardiomyopathy is a disease of the myocardium. There arethree types: dilated, hypertrophic, and restrictive (see Chap. 29).Dilated cardiomyopathy, the most common type of cardio-myopathy, causes diffuse cellular necrosis, leading to decreasedcontractility (systolic failure). Dilated cardiomyopathy can be id-iopathic (unknown cause), or it can result from an inflammatoryprocess, such as myocarditis, from pregnancy, or from a cytotoxicagent, such as alcohol or adriamycin. Hypertrophic cardiomy-opathy and restrictive cardiomyopathy lead to decreased disten-sibility and ventricular filling (diastolic failure). Usually, HF dueto cardiomyopathy becomes chronic. However, cardiomyopathyand HF may resolve after the end of pregnancy or with the ces-sation of alcohol ingestion.

Systemic or pulmonary hypertension increases afterload (resis-tance to ejection), which increases the workload of the heart andleads to hypertrophy of myocardial muscle fibers; this can be con-sidered a compensatory mechanism because it increases contrac-tility. However, the hypertrophy may impair the heart’s ability tofill properly during diastole.

Valvular heart disease is also a cause of HF. The valves ensurethat blood flows in one direction. With valvular dysfunction,blood has increasing difficulty moving forward, increasing pres-sure within the heart and increasing cardiac workload, leading todiastolic HF. Chapter 29 discusses the effects of valvular heartdisease.

Several systemic conditions contribute to the developmentand severity of HF, including increased metabolic rate (eg, fever,thyrotoxicosis), iron overload (eg, from hemochromatosis),hypoxia, and anemia (serum hematocrit less than 25%). All ofthese conditions require an increase in CO to satisfy the sys-temic oxygen demand. Hypoxia or anemia also may decrease thesupply of oxygen to the myocardium. Cardiac dysrhythmias maycause HF, or they may be a result of HF; either way, the alteredelectrical stimulation impairs the myocardial contraction and de-creases the overall efficiency of myocardial function. Other factors,such as acidosis (respiratory or metabolic), electrolyte abnor-malities, and antiarrhythmic medications, can worsen the myo-cardial dysfunction.

Clinical ManifestationsThe clinical manifestations produced by the different types of HF(systolic, diastolic, or both) are similar (Chart 30-2) and there-fore do not assist in differentiating the types of HF. The signs andsymptoms of HF are most often described in terms of the effecton the ventricles. Left-sided heart failure (left ventricular fail-ure) causes different manifestations than right-sided heart fail-ure (right ventricular failure). Chronic HF produces signs andsymptoms of failure of both ventricles. Although dysrhythmias(especially tachycardias, ventricular ectopic beats, or atrioven-tricular [AV] and ventricular conduction defects) are common inHF, they may also be a result of treatments used in HF (eg, sideeffect of digitalis).

LEFT-SIDED HEART FAILUREPulmonary congestion occurs when the left ventricle cannot pumpthe blood out of the ventricle to the body. The increased left ven-tricular end-diastolic blood volume increases the left ventricularend-diastolic pressure, which decreases blood flow from the leftatrium into the left ventricle during diastole. The blood volumeand pressure in the left atrium increases, which decreases bloodflow from the pulmonary vessels. Pulmonary venous blood vol-ume and pressure rise, forcing fluid from the pulmonary capillar-

ies into the pulmonary tissues and alveoli, which impairs gas ex-change. These effects of left ventricular failure have been referredto as backward failure. The clinical manifestations of pulmonaryvenous congestion include dyspnea, cough, pulmonary crackles,and lower-than-normal oxygen saturation levels. An extra heartsound, S3, may be detected on auscultation.

Dyspnea, or shortness of breath, may be precipitated by mini-mal to moderate activity (dyspnea on exertion [DOE]); dyspneaalso can occur at rest. The patient may report orthopnea, difficultyin breathing when lying flat. Patients with orthopnea usually pre-fer not to lie flat. They may need pillows to prop themselves up inbed, or they may sit in a chair and even sleep sitting up. Some pa-tients have sudden attacks of orthopnea at night, a conditionknown as paroxysmal nocturnal dyspnea (PND). Fluid that ac-cumulated in the dependent extremities during the day begins tobe reabsorbed into the circulating blood volume when the personlies down. Because the impaired left ventricle cannot eject the in-creased circulating blood volume, the pressure in the pulmonarycirculation increases, causing further shifting of fluid into the alve-oli. The fluid filled alveoli cannot exchange oxygen and carbondioxide. Without sufficient oxygen, the patient experiences dys-pnea and has difficulty getting an adequate amount of sleep.

The cough associated with left ventricular failure is initiallydry and nonproductive. Most often, patients complain of a dryhacking cough that may be mislabeled as asthma or chronic ob-structive pulmonary disease (COPD). The cough may becomemoist. Large quantities of frothy sputum, which is sometimes

Chart 30-2 • ASSESSMENT

Signs and Symptoms of Heart Failure

GeneralPale, cyanotic skin (with decreased perfusion to extremities)Dependent edema (with increased venous pressure)Deceased activity tolerance

CardiovascularApical impulse, enlarged and left lateral displacement (with cardiac

enlargement)Third heart sound (S3)Murmurs (with valvular dysfunction)TachycardiaIncreased jugular venous distention (JVD)

CerebrovascularLightheadnessDizzinessConfusion

GastrointestinalNausea and anorexiaEnlarged, pulsatile liverAscitesHepatojugular test, increased (with increased right ventricular

filling pressure)

RenalDecreased urinary frequency during the dayNocturia

RespiratoryDyspnea on exertionOrthopneaParoxysmal nocturnal dyspneaBilateral crackles that do not clear with cough


pink (blood tinged), may be produced, usually indicating severepulmonary congestion (pulmonary edema).

Adventitious breath sounds may be heard in various lobes of thelungs. Usually, bi-basilar crackles that do not clear with coughingare detected in the early phase of left ventricular failure. As the fail-ure worsens and pulmonary congestion increases, crackles may beauscultated throughout all lung fields. At this point, a decrease inoxygen saturation may occur.

In addition to increased pulmonary pressures that cause de-creased oxygenation, the amount of blood ejected from the leftventricle may decrease, sometimes called forward failure. Thedominant feature in HF is inadequate tissue perfusion. The di-minished CO has widespread manifestations because not enoughblood reaches all the tissues and organs (low perfusion) to pro-vide the necessary oxygen. The decrease in SV can also lead tostimulation of the sympathetic nervous system, which further im-pedes perfusion to many organs.

Blood flow to the kidneys decreases, causing decreased perfu-sion and reduced urine output (oliguria). Renal perfusion pres-sure falls, which results in the release of renin from the kidney.Release of renin leads to aldosterone secretion. Aldosterone se-cretion causes sodium and fluid retention, which further increasesintravascular volume. However, when the patient is sleeping, thecardiac workload is decreased, improving renal perfusion, whichthen leads to frequent urination at night (nocturia).

Decreased CO causes other symptoms. Decreased gastro-intestinal perfusion causes altered digestion. Decreased brain per-fusion causes dizziness, lightheadedness, confusion, restlessness,and anxiety due to decreased oxygenation and blood flow. As anx-iety increases, so does dyspnea, enhancing anxiety and creating avicious cycle. Stimulation of the sympathetic system also causesthe peripheral blood vessels to constrict, so the skin appears paleor ashen and feels cool and clammy.

The decrease in the ejected ventricular volume causes thesympathetic nervous system to increase the heart rate (tachy-cardia), often causing the patient to complain of palpitations.The pulses become weak and thready. Without adequate CO,the body cannot respond to increased energy demands, and thepatient is easily fatigued and has decreased activity tolerance.Fatigue also results from the increased energy expended in breath-ing and the insomnia that results from respiratory distress, cough-ing, and nocturia.

RIGHT-SIDED HEART FAILUREWhen the right ventricle fails, congestion of the viscera and theperipheral tissues predominates. This occurs because the rightside of the heart cannot eject blood and cannot accommodateall the blood that normally returns to it from the venous circu-lation. The increase in venous pressure leads to jugular vein dis-tention ( JVD).

The clinical manifestations that ensue include edema of thelower extremities (dependent edema), hepatomegaly (enlarge-ment of the liver), distended jugular veins, ascites (accumulationof fluid in the peritoneal cavity), weakness, anorexia and nausea,and paradoxically, weight gain due to retention of fluid.

Edema usually affects the feet and ankles, worsening whenthe patient stands or dangles the legs. The swelling decreaseswhen the patient elevates the legs. The edema can graduallyprogress up the legs and thighs and eventually into the externalgenitalia and lower trunk. Edema in the abdomen, as evidencedby increased abdominal girth, may be the only edema present.Sacral edema is not uncommon for patients who are on bed rest,because the sacral area is dependent. Pitting edema, in which

indentations in the skin remain after even slight compressionwith the fingertips (Fig. 30-2), is obvious only after retention ofat least 4.5 kg (10 lb) of fluid (4.5 liters).

Hepatomegaly and tenderness in the right upper quadrant ofthe abdomen result from venous engorgement of the liver. The in-creased pressure may interfere with the liver’s ability to perform(secondary liver dysfunction). As hepatic dysfunction progresses,pressure within the portal vessels may rise enough to force fluidinto the abdominal cavity, a condition known as ascites. This col-lection of fluid in the abdominal cavity may increase pressure onthe stomach and intestines and cause gastrointestinal distress. He-patomegaly may also increase pressure on the diaphragm, causingrespiratory distress.

Anorexia (loss of appetite) and nausea or abdominal pain re-sults from the venous engorgement and venous stasis within theabdominal organs. The weakness that accompanies right-sidedHF results from reduced CO, impaired circulation, and in-adequate removal of catabolic waste products from the tissues.

Assessment and Diagnostic FindingsHF may go undetected until the patient presents with signsand symptoms of pulmonary and peripheral edema (congestion),which can lead the physician to make a preliminary diagnosis ofCHF. However, the physical signs that suggest HF may also occurwith other diseases, such as renal failure, liver failure, oncologicconditions, and COPD. If further assessment and evaluation are

A

B

FIGURE 30-2 Example of pitting edema. (A) The nurse applies fingerpressure to an area near the ankle. (B) When the pressure is released, an in-dentation remains in the edematous tissue. Photographs © B. Proud.

not completed, these patients may be treated for HF inappropri-ately. The term congestive heart failure (CHF) means the patienthas a fluid overload condition (congestion) that may or may notbe caused by HF. CHF is caused by HF when ventricular dys-function (systolic, diastolic, or both) has been identified. Assess-ment of ventricular function is an essential part of the initialdiagnostic workup.

An echocardiogram is usually performed to confirm the diag-nosis of HF, assist in the identification of the underlying cause, anddetermine the patient’s ejection fraction, which assists in identifi-cation of the type and severity of HF. This information may alsobe obtained noninvasively by radionuclide ventriculography or in-vasively by ventriculogram as part of a cardiac catheterization pro-cedure. A chest x-ray and an electrocardiogram (ECG) are obtainedto assist in the diagnosis and to determine the underlying cause ofHF. Laboratory studies usually completed in the initial workup in-clude serum electrolytes, blood urea nitrogen (BUN), creatinine,B-type natriuretic peptide (BNP), thyroid-stimulating hormone(TSH), a complete blood cell count (CBC), and routine urinaly-sis. The results of these laboratory studies assist in determining theunderlying cause and in establishing a baseline from which to mea-sure effects of treatment. Exercise testing or cardiac catheterizationmay be performed to determine whether coronary artery diseaseand cardiac ischemia are causing the HF.

Ventricular function should be determined before dischargefrom a hospital of patients with acute myocardial infarction (MI)who are at risk for the development of HF. Patients who are at lowrisk for HF are those who meet all of the following criteria: no pre-vious myocardial infarction, inferior myocardial infarction, small(less than two to four times normal) increase in cardiac enzymes,no Q waves on the ECG, and an uncomplicated clinical course(AHCPR, 1994). Evaluation of ventricular function may also beperformed for patients whose initial assessment of HF suggestednoncardiac causes but who failed to respond to treatment.

Medical ManagementA critical step in the management of HF is early identification anddocumentation of the type of HF. Medical management, especiallythe pharmacologic therapy, varies with the type of HF. The basicobjectives in treating patients with HF are the following:

• Eliminate or reduce any etiologic contributory factors, es-pecially those that may be reversible, such as atrial fibrilla-tion or excessive alcohol ingestion.

• Reduce the workload on the heart by reducing afterload andpreload.

Managing the patient with HF includes providing generalcounseling and education about sodium restriction, monitoringdaily weights and other signs of fluid retention, encouraging reg-ular exercise, and recommending avoidance of excessive fluid in-take, alcohol, and smoking. Medications are prescribed based onthe patient’s type and severity of HF. Oxygen therapy is based onthe degree of pulmonary congestion and resulting hypoxia. Somepatients may need supplemental oxygen therapy only during ac-tivity. Others may require hospitalization and endotracheal in-tubation. If the patient has underlying coronary artery disease,coronary artery revascularization with percutaneous translumi-nal coronary angioplasty (PTCA) or bypass surgery (see Chap. 28)may be considered. If the patient’s condition is unresponsive toadvanced aggressive medical therapy, innovative therapies, in-cluding mechanical assist devices and transplantation, may beconsidered.

Cardiac resynchronization, involving the use of left ventricu-lar and biventricular pacing, is a treatment for HF with electricalconduction defects. Left bundle branch block (LBBB) is fre-quently found in patients with systolic dysfunction. LBBB occurswhen the electrical impulse, which normally depolarizes the rightand left bundle branches at the same time, depolarizes the rightbundle branch but not the left bundle branch. The dyssynchro-nous electrical stimulation of the ventricles causes the right ven-tricle to contract before the left ventricle, which can lead tofurther decreased ejection fraction (Gerber et al., 2001). Use of apacing device (eg, Medtronic InSync), with leads placed on theinner wall of the right atrium and right ventricle and on the outerwall of the left ventricle, provides synchronized electrical stimu-lation to the heart. In one study, 63% of the patients who had re-ceived these devices showed improvement in clinical status,including NYHA functional class and global assessment, com-pared with 38% of placebo patients (Abraham, 2002).

PHARMACOLOGIC THERAPYSeveral medications are indicated for systolic HF. Medicationsfor diastolic failure depend on the underlying condition, such ashypertension (see Chap. 32) or valvular dysfunction (see Chap. 29).If the patient is in mild systolic failure, an ACE inhibitor usuallyis prescribed. If the patient is unable to continue an ACE inhibitor(eg, because of development of renal impairment as evidenced byelevated serum creatinine or persistent serum potassium levels of5.5 mEq/L or above), an angiotensin II receptor blocker (ARB)or hydralazine and isosorbide dinitrate are considered as part ofthe treatment plan. A diuretic is added if signs of fluid overloaddevelop. Digitalis is added to ACE inhibitors if the symptomscontinue. Although previously contraindicated in HF, specificbeta-blockers decrease mortality and morbidity if added to theinitial medications. Spironolactone, a weak diuretic may also beadded for persistent symptoms.

Angiotensin-Converting Enzyme Inhibitors. ACE inhibitors(ACE-Is) have a pivotal role in the management of HF due to sys-tolic dysfunction. They have been found to relieve the signs andsymptoms of HF and significantly decrease mortality and mor-bidity (when used to treat a symptomatic patient) by inhibitingneurohormonal activation (CONSENSUS Trial Study Group,1987; SOLVD Investigators, 1992). Available as oral and intra-venous medications, ACE-Is promote vasodilation and diuresisby decreasing afterload and preload. By doing so, they decrease theworkload of the heart. Vasodilation reduces resistance to left ven-tricular ejection of blood, diminishing the heart’s workload andimproving ventricular emptying. In promoting diuresis, ACE-Isdecrease the secretion of aldosterone, a hormone that causes thekidneys to retain sodium. ACE-Is stimulate the kidneys to excretesodium and fluid (while retaining potassium), thereby reducing leftventricular filling pressure and decreasing pulmonary congestion.ACE-Is may be the first medication prescribed for patients in mildfailure—patients with fatigue or dyspnea on exertion but withoutsigns of fluid overload and pulmonary congestion.

Results from studies (Clement et al., 2000; NETWORKInvestigators, 1998) to identify the specific dose to achieve thiseffect are equivocal, although one large study showed significantreductions in death and hospitalization with higher doses (Packeret al., 1999). However, it is recommended to start at a low doseand increase every 2 weeks until the optimal dose is achieved andthe patient is hemodynamically stable. The final maintenancedose depends on the patient’s blood pressure, fluid status, renalstatus, and degree of cardiac failure.



Patients receiving ACE-I therapy are monitored for hypoten-sion, hypovolemia, hyponatremia, and alterations in renal func-tion, especially if they are also receiving diuretics. When to observefor these effects and for how long depends on the onset, peak, andduration of the medication. Table 30-3 identifies several types ofACE-Is and their pharmacokinetics. Hypotension is most likelyto develop from ACE-I therapy in patients older than age 75 andin those with a systolic blood pressure of 100 mm Hg or less, aserum sodium level of less than 135 mEq/L, or severe cardiac fail-ure. Adjusting the dose or type of diuretic in response to the pa-tient’s blood pressure and renal function may allow for continuedincreases in the dosage of ACE-Is.

Because ACE-Is cause the kidneys to retain potassium, thepatient who is also receiving a diuretic may not need to take oralpotassium supplements. However, patients receiving potassium-sparing diuretics (which do not cause potassium loss with diuresis)must be carefully monitored for hyperkalemia, an increased levelof potassium in the blood. Before the initiation of the ACE-I, hy-perkalemic and hypovolemic states must be corrected. ACE-Is maybe discontinued if the potassium remains above 5.0 mEq/L or ifthe serum creatinine is 3.0 mg/dL and continues to increase. Otherside effects of ACE-Is include a dry, persistent cough that may notrespond to cough suppressants. However, the cough could also in-dicate a worsening of ventricular function and failure. Rarely, thecough indicates angioedema. If angioedema affects the oropha-ryngeal area and impairs breathing, the ACE-I must be stoppedimmediately.

Angiotensin II Receptor Blockers (ARBs). Although their actionis different than that of ACE-Is, ARBs (eg, losartan [Cozaar]) havea similar hemodynamic effect as ACE-Is: lowered blood pressureand lowered systemic vascular resistance. Whereas ACE-Is blockthe conversion of angiotensin I to angiotensin II, ARBs block theeffects of angiotensin II at the angiotensin II receptor. ACE-Isand ARBs also have similar side effects: hyperkalemia, hypoten-sion, and renal dysfunction. ARBs are usually prescribed whenpatients are not able to tolerate ACE-Is.

Hydralazine and Isosorbide Dinitrate. A combination of hy-dralazine (Apresoline) and isosorbide dinitrate (Dilatrate-SR,Isordil, Sorbitrate) may be another alternative for patients whocannot take ACE-Is. Nitrates (eg, isosorbide dinitrate) cause ve-

nous dilation, which reduces the amount of blood return to theheart and lowers preload. Hydralazine lowers systemic vascularresistance and left ventricular afterload. It has also been shown tohelp avoid the development of nitrate tolerance. As with ARBs,this combination of medications is usually used when patients arenot able to tolerate ACE-Is.

Beta-Blockers. When used with ACE-Is, beta-blockers, such ascarvedilol (Coreg), metoprolol (Lopressor, Toprol), or bisopro-lol (Zebeta), have been found to reduce mortality and morbidityin NYHA class II or III HF patients by reducing the cytotoxic ef-fects from the constant stimulation of the sympathetic nervoussystem (Beta-Blocker Evaluation of Survival Trial [BEST] Inves-tigators, 2001; CIBIS-II Investigators and Committees, 1999;MERIT, 1999; Packer et al., 1996; Packer et al., 2001). Theseagents have also been recommended for patients with asympto-matic systolic dysfunction, such as after acute myocardial infarc-tion or revascularization to prevent the onset of symptoms of HF.However, beta-blockers may also produce many side effects, in-cluding exacerbation of HF. The side effects are most common inthe initial few weeks of treatment. The most frequent side effectsare dizziness, hypotension, and bradycardia. To minimize theseside effects, staggering the administration of the beta-blockerwith the ACE-I is recommended. Because of the side effects, beta-blockers are initiated only after stabilizing the patient and ensuringa euvolemic (normal volume) state. They are titrated slowly (every2 weeks), with close monitoring at each increase in dose. If thepatient develops symptoms during the titration phase, treat-ment options include increasing the diuretic, reducing the doseof ACE-I, or decreasing the dose of the beta-blocker.

An important nursing role during titration is educating the pa-tient about the potential worsening of symptoms during the earlyphase of treatment, and that improvement may take several weeks.It is very important that nurses provide support to patients goingthrough this symptom-provoking phase of treatment. Becausebeta-blockade can cause bronchiole constriction, a beta1-selectivebeta-blocker (ie, one that primarily blocks the beta-adrenergic re-ceptor sites in the heart), such as metoprolol (Lopressor, Toprol),is recommended for patients with well-controlled, mild to moder-ate asthma. However, these patients need to be monitored closelyfor increased asthma symptoms. Any type of beta-blocker is con-traindicated in patients with severe or uncontrolled asthma.

Table 30-3 • Angiotensin-Converting Enzyme (ACE) Inhibitors

PHARMACOKINETICS

ACE INHIBITOR Onset Peak (hr) Duration (hr) NURSING CONSIDERATIONS

benazepril (Lotensin)captopril (Capoten)enalapril (Vasotec)enalaprilat (Vasotec I.V.)fosinopril (Monopril)lisinopril (Prinival, Zestril)moexipril (Univasc)quinapril (Accupril)ramipril (Altace)trandolapril (Mavik)

within 1 hr15–60 min1 hr15 minwithin 1 hr1 hr1 hrwithin 1 hr1–2 hrwithin 30 min

2–41–1.54–61–42–663–62–44–62–4

246–12*246242424up to 24*24> 8 days

Monitor blood pressure, urine output, and electrolyte levels.Monitor serum creatinine and urine creatinine clearance.Monitor for development of cough that is resistant to cough

suppressants.Teach patient to change positions gradually and to report

signs of dizziness or lethargy.Instruct patient to weigh self daily and to report rapid weight

gain and significant feet and hand swelling.

*Duration of effect is related to the dose.


Diuretics. Diuretics are medications used to increase the rate ofurine production and the removal of excess extracellular fluid fromthe body. Of the types of diuretics prescribed for patients withedema from HF, three are most common: thiazide, loop, andpotassium-sparing diuretics. These medications are classifiedaccording to their site of action in the kidney and their effects onrenal electrolyte excretion and reabsorption. Thiazide diuretics,such as metolazone (Mykrox, Zaroxolyn), inhibit sodium andchloride reabsorption mainly in the early distal tubules. They alsoincrease potassium and bicarbonate excretion. Loop diuretics, suchas furosemide (Lasix), inhibit sodium and chloride reabsorptionmainly in the ascending loop of Henle. Patients with signs andsymptoms of fluid overload should be started on a diuretic, athiazide for those with mild symptoms or a loop diuretic for patientswith more severe symptoms or with renal insufficiency (Brater,1998). Both types of diuretics may be used for those in severe HF

and unresponsive to a single diuretic. These medications may notbe necessary if the patient responds to activity recommendations,avoidance of excessive fluid intake (<2 quarts/day), and a low-sodium diet (eg, <2 g/day).

Spironolactone (Aldactone) is a potassium-sparing diuretic thatinhibits sodium reabsorption in the late distal tubule and collect-ing duct. It has been found to be effective in reducing mortality andmorbidity in NYHA class III and IV HF patients when added toACE-Is, loop diuretics, and digoxin. Serum creatinine and potas-sium levels are monitored frequently (eg, within the first week andthen every 4 weeks) when this medication is first administered.

Side effects of diuretics include electrolyte imbalances, symp-tomatic hypotension (especially with overdiuresis), hyperuricemia(causing gout), and ototoxicity. Dosages depend on the indica-tions, patient age, clinical signs and symptoms, and renal function.Table 30-4 lists commonly used diuretics, dosages, and pharma-

Table 30-4 • Diuretic Medications Used to Treat Heart Failure

DIURETIC USUAL ADULT DOSE ONSET (HR) PEAK (HR) DURATION (HR)

Thiazide Diureticsbendroflumethiazide

(Naturetin)benzthiazide (Exna)chlorothiazide (Diuril)

chlorthalidone (Hygroton)

hydrochlorothiazide(HydroDIURIL, Esidrix,Oretic)

hydroflumethiazide(Diucardin, Saluron)

methyclothiazide (Enduron)metolazone (Zaroxolyn,

Mykrox)polythiazide (Renese)

quinethazone (Hydromox)

trichlormethiazide (Metahy-drin, Naqua)

Loop Diureticsbumetanide (Bumex)

ethacrynic acid (Edecrin)

furosemide (Lasix)

torsemide (Demadex)

Potassium-Sparing Diureticsamiloride (Midamor)spironolactone (Aldactone)triamterene (Dyrenium)

2.5–20 mg in single or divided dose, once a day, once every other day, or once a day for 3–5 days per week

12.5–200 mg in single or divided doseOral: 0.25–2 g as single or divided dose; may be given on

alternate daysIV: 0.5–1 g in single or divided dose (note: avoid

extravasation)12.5–200 mg once a day, once every other day, or once a

day for 3 days per week12.5–200 mg as single or divided dose once a day, once

every other day, or once a day for 3–5 days per week

25–200 mg as single or divided dose once a day, once every other day, or once a day for 3–5 days per week

2.5–10 mg once a dayZaroxolyn: 2.5–20 mg once a day

Mykrox: 0.5–1 mg once a day1–4 mg once a day, once every other day, or once a day

for 3–5 days per week25–100 mg as single or divided dose; rarely, 200 mg once

a day1–4 mg once or twice a day

0.5–2 mg once, twice or three times a day; may be given on alternate days or once every 3 days

0.5–1 mg over 2 min; repeat every 2–3 h; a continuous infusion may be given at a rate of 1 mg/h.

50–400 mg as single or divided dose0.5–1 mg/kg (max 100 mg) over several min; may be

repeated within 2–6 h; repeat every hour in emergencies20–600 mg as single daily dose, divided daily dose, as a

dose given every other day or given once a day for2–4 days per week

20–200 mg (max 6 mg/kg) given at a rate of 4 mg/min; after response obtained, given once or twice a day

5–200 mg as a daily single doseIV and oral doses are equivalent. Give IV over 2 min.

5–20 mg daily as single dose25–400 mg as single dose or divided up to 4 doses50–300 mg as single dose

2

22

15 min

2

2

2

21

2

2

2

30–60 min

5–10 min

<30 min<5 min

<1

<5 min

<1<10 min

224–482–4

4

4–64

30 min

2–6

4–6

4

62

6

6

6

1–2

15–30 min

215–30 min

1–2

30 min

1–2<1

6–1048–726–8

12–16

16–1816–18

24–72

12–16

12–16

2412–24

24–28

18–24

24

4–6

1⁄2–1

6–82

6–8

2

6–86–8

2448–7212–16


cokinetic properties. Careful patient monitoring and dose adjust-ments are necessary to balance the effectiveness with the side ef-fects of therapy. Diuretics greatly improve the patient’s symptoms,but they do not prolong life.

Digitalis. The most commonly prescribed form of digitalis for pa-tients with HF is digoxin (Lanoxin). The medication increases theforce of myocardial contraction and slows conduction through theAV node. It improves contractility, increasing left ventricularoutput. The medication also enhances diuresis, which removesfluid and relieves edema. The effect of a given dose of medicationdepends on the state of the myocardium, electrolyte and fluid

balance, and renal and hepatic function. Although digitalis doesnot decrease the mortality rate, it is effective in decreasing thesymptoms of systolic HF and in increasing the patient’s ability toperform activities of daily living (Digitalis Investigation Group,1997). It also has been shown to significantly decrease hospital-ization rates and emergency room visits for NYHA class II and IIIHF patients (Uretsky et al., 1993).

A key concern associated with digitalis therapy is digitalis tox-icity. Chart 30-3 summarizes the actions and uses of digitalis alongwith the nursing surveillance required when it is administered.The patient is observed for the effectiveness of digitalis ther-apy: lessening dyspnea and orthopnea, decrease in pulmonary

Chart 30-3 • PHARMACOLOGYDigoxin Use and Toxicity in Heart Failure

Digoxin, a cardiac glycoside derived from digitalis, is used for patientswith systolic HF, atrial fibrillation, and atrial flutter. Digoxin improvescardiac function as follows:

• Increases the force of myocardial contraction• Slows cardiac conduction through the AV node and therefore slows

the ventricular rate in instances of supraventricular dysrhythmias• Increases cardiac output by enhancing the force of ventricular

contraction• Promotes diuresis by increasing cardiac output.

The therapeutic level is usually 0.5 to 2.0 ng/mL. Blood samples areusually obtained and analyzed to determine digitalis concentration atleast 6 to 10 hours after the last dose. Toxicity may occur despite nor-mal serum levels, and recommended dosages vary considerably.

PreparationsDigoxin• Tablets: 0.125, 0.25, 0.5 mg (Lanoxin)• Capsules: 0.05, 0.1, 0.2 mg (Lanoxicaps)• Elixir: 0.05 mg/mL (Lanoxin Pediatric elixir)• Injection: 0.25 mg/mL, 0.1 mg/mL (Lanoxin)

Digoxin ToxicityA serious complication of digoxin therapy is toxicity. The incidenceis high, and toxicity may occur even though the serum digoxin levelremains within a normal range. Diagnosis of digoxin toxicity is basedon the patient’s clinical symptoms, which include the following:

• Fatigue, depression, malaise, anorexia, nausea, and vomiting(early effects of digitalis toxicity)

• Changes in heart rhythm: new onset of regular rhythm or newonset of irregular rhythm

• ECG changes indicating SA or AV block; new onset of irregular rhythm indicating ventricular dysrhythmias; and atrial tachycardiawith block, junctional tachycardia, and ventricular tachycardia

Reversal of ToxicityDigoxin toxicity is treated by holding the medication while monitor-ing the patient’s symptoms and serum digoxin level. If the toxicity issevere, digoxin immune FAB (Digibind) may be prescribed. Digibindbinds with digoxin and makes it unavailable for use. The Digibinddosage is based on the digoxin level and the patient’s weight. Serumdigoxin values are not accurate for several days after administrationof Digibind because they do not differentiate between bound andunbound digoxin. Because Digibind quickly decreases the amountof available digoxin, an increase in ventricular rate due to atrial fi-brillation and worsening of symptoms of HF may ensue shortly afterits administration.

Nursing Considerations and Actions1. Assess the patient’s clinical response to digoxin therapy by evalu-

ating relief of symptoms such as dyspnea, orthopnea, crackles, he-patomegaly, and peripheral edema.

2. Monitor serum potassium levels in patients receiving digoxin,especially those receiving both digoxin and diuretics. Anundetected, uncorrected potassium imbalance predisposes patients to digoxin toxicity and dysrhythmias.

3. Assess for symptoms of electrolyte depletion: lassitude, apathy, mental confusion, anorexia, decreasing urinary output,azotemia.

4. Monitor the patient for factors that increase the risk of toxicity:• Oral antibiotics, quinidine, amiodarone, calcium channel

blocker therapy (See Table 27-1).• Decreased potassium level (hypokalemia), which increases the

action of digoxin and which may be caused by malnutrition,diarrhea, vomiting, or prolonged muscle wasting

• Impaired renal function, particularly in patients age 65 andolder with decreased renal clearance.

5. Before administering digoxin, it is standard nursing practice to as-sess apical heart rate. When the patient’s rhythm is atrial fibrilla-tion and the heart rate is less than 60, or the rhythm becomesregular, the nurse may withhold the medication and notify thephysician, because these signs indicate the development of AVconduction block. Although withholding digoxin is a commonpractice, the medication does not need to be withheld for a heartrate of less than 60 if the patient is in sinus rhythm becausedigoxin does not affect sinoatrial node automaticity. Measuringthe PR interval for a patient with cardiac monitoring is moreimportant than the apical pulse in determining whether digoxinshould be held.

Note: If monitoring discloses that the patient is in sinusrhythm, the nurse monitors the patient’s PR interval instead ofthe patient’s heart rate. If the patient is in atrial fibrillation, thenurse monitors for the development of regular R-R intervals, indicating AV block.

6. Monitor for gastrointestinal side effects: anorexia, nausea, vomiting,abdominal pain and distention.

7. Monitor for neurologic side effects: headache, malaise, night-mares, forgetfulness, social withdrawal, depression, agitation,confusion, paranoia, hallucinations, decreased visual acuity, yellow or green halo around objects (especially lights), or“snowy” vision.

8. Observe for and anticipate potential drug interactions whenother medications are added to the patient’s regimen. This is an important step in preventing toxicity. For example, anti-arrhythmic and antibiotic medications may increase the amount of digoxin available to the patient. Diuretics may decrease the amount of potassium and increase the availabilityof digoxin. In addition, because digoxin is eliminated by thekidneys, renal function (serum creatinine and urine creatinineclearance) are monitored carefully.


crackles on auscultation, relief of peripheral edema, weight loss, andincrease in activity tolerance. The serum potassium level is mea-sured at intervals because diuresis may have caused hypokalemia.The effect of digitalis is enhanced in the presence of hypokalemia,so digitalis toxicity may occur. Serum digoxin levels are obtainedonce each year or more frequently if there have been changes inthe patient’s medications, renal function, or symptoms.

Calcium Channel Blockers. First-generation calcium channelblockers, such as verapamil (Calan, Isoptin, Verelan), nifedipine(Adalat, Procardia), and diltiazem (Cardizem, Dilacor, Tiazac),are contraindicated in patients with systolic dysfunction, althoughthey may be used in patients with diastolic dysfunction. Am-lodipine (Norvasc) and felodipine (Plendil), dihydropyridinecalcium channel blockers, cause vasodilation, reducing systemicvascular resistance. They may be used to improve symptoms es-pecially in patients with nonischemic cardiomyopathy, althoughthey have no effect on mortality.

Other Medications. Anticoagulants may be prescribed, especiallyif the patient has a history of an embolic event or atrial fibrillationor mural thrombus is present. Other medications such as anti-anginal medications may be given to treat the underlying cause ofHF. Nonsteroidal anti-inflammatory drugs (NSAIDs), such asibuprophen (Aleve, Advil, Motrin) should be avoided (Page &Henry, 2000). They can increase systemic vascular resistance anddecrease renal perfusion, especially in the elderly. For similar rea-sons, use of decongestants should be avoided.

NUTRITIONAL THERAPYA low-sodium (≤2 to 3 g/day) diet and avoidance of excessiveamounts of fluid are usually recommended. Although it has notbeen shown to affect the mortality rate, this recommendation re-duces fluid retention and the symptoms of peripheral and pul-monary congestion. The purpose of sodium restriction is to decreasethe amount of circulating volume, which would decrease the needfor the heart to pump that volume. A balance needs to be achievedbetween the ability of the patient to alter the diet and the amountof medications that are prescribed. Any change in diet needs to bedone with consideration of good nutrition as well as the patient’slikes, dislikes, and cultural food patterns.

Nursing ManagementThe nurse is responsible for administering the medications andfor assessing their beneficial and detrimental effects to the patient.It is the balance of these effects that determines the type anddosage of pharmacologic therapy. Nursing actions to evaluatetherapeutic effectiveness include the following:

• Keeping an intake and output record to identify a negativebalance (more output than input)

• Weighing the patient daily at the same time and on thesame scale, usually in the morning after urination; moni-toring for a 2- to 3-lb gain in a day or 5-lb gain in week

• Auscultating lung sounds at least daily to detect an increaseor decrease in pulmonary crackles

• Determining the degree of JVD• Identifying and evaluating the severity of dependent edema• Monitoring pulse rate and blood pressure, as well as moni-

toring for postural hypotension and making sure that thepatient does not become hypotensive from dehydration

• Examining skin turgor and mucous membranes for signs ofdehydration

• Assessing symptoms of fluid overload (eg, orthopnea, parox-ysmal nocturnal dyspnea, and dyspnea on exertion) andevaluating changes

MONITORING AND MANAGING POTENTIAL COMPLICATIONSProfuse and repeated diuresis can lead to hypokalemia (ie, potas-sium depletion). Signs are weak pulse, faint heart sounds, hypo-tension, muscle flabbiness, diminished deep tendon reflexes, andgeneralized weakness. Hypokalemia poses new problems for the pa-tient with HF because it markedly weakens cardiac contractions.In patients receiving digoxin, hypokalemia can lead to digitalis tox-icity. Digitalis toxicity and hypokalemia increase the likelihood ofdangerous dysrhythmias (see Chart 30-3). Low levels of potassiummay also indicate a low level of magnesium, which can add to therisk for dysrhythmias. Hyperkalemia may also occur, especiallywith the use of ACE-Is or ARBs and spironolactone.

NURSING ALERT The sources of sodium should be specified in describing the regimen, rather than simply saying “low-salt” or “salt-free,” and the quantity should be indicated in milligrams. Salt is not100% sodium; there are 393 mg of sodium in 1 g (1000 mg) of salt.

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NURSING ALERT To reduce the risk for hypokalemia, thenurse advises patients to increase their dietary intake of potassium. Dried apricots, bananas, beets, figs, orange ortomato juice, peaches, and prunes (dried plums), potatoes,raisins, spinach, squash, and watermelon are good dietarysources of potassium. An oral potassium supplement (potassium chloride) may also be prescribed for patients receiving diuretic medications. If the patient is at risk for hyperkalemia, the nurse advises the patient to avoid the aboveproducts, including salt substitutes.

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NURSING ALERT Grapefruit (fresh and juice) is a good dietarysource of potassium but has serious drug–food interactions. Patients are advised to consult their physician or pharmacist before including grapefruit in their diet. !

NURSING ALERT Periodic assessment of the patient’s electrolytelevels will alert health team members to hypokalemia, hypomagne-semia, and hyponatremia. Serum levels are assessed frequently when the patient starts diuretic therapy and then usually every 3 to12 months. It is important to remember that serum potassium levelsdo not always indicate the total amount of potassium within the body.

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Prolonged diuretic therapy may also produce hyponatremia(deficiency of sodium in the blood), which results in apprehen-sion, weakness, fatigue, malaise, muscle cramps and twitching,and a rapid, thready pulse.

Other problems associated with diuretic administration arehyperuricemia (excessive uric acid in the blood), volume deple-tion from excessive urination, and hyperglycemia.

Gerontologic Considerations

Several normal changes that occur with aging increase the frequencyof diastolic HF: increased systolic blood pressure, increased ventric-


ular wall thickness, increased atrial size, and increased myocardial fi-brosis. Elderly people may present with atypical signs and symptoms:fatigue, weakness, and somnolence. Decreased renal functionmakes the elderly patient resistant to diuretics and more sensitiveto changes in volume, especially with diastolic dysfunction. The ad-ministration of diuretics to elderly men requires nursing surveil-lance for bladder distention caused by urethral obstruction from anenlarged prostate gland. The bladder may be assessed with an ul-trasound scanner, or the suprapubic area palpated for an oval massand percussed for dullness, indicative of bladder fullness,

NURSING PROCESS: THE PATIENT WITH HEART FAILUREAssessmentThe nursing assessment for the patient with HF focuses on ob-serving for effectiveness of therapy and for the patient’s ability tounderstand and implement self-management strategies. Signs andsymptoms of pulmonary and systemic fluid overload are recordedand reported immediately so that adjustments can be made in ther-apy. The nurse also explores the patient’s emotional response to thediagnosis of HF, a chronic illness.

HEALTH HISTORYThe nurse explores sleep disturbances, particularly sleep suddenly in-terrupted by shortness of breath. The nurse also asks about the num-ber of pillows needed for sleep (an indication of orthopnea), activitiesof daily living, and the activities that cause shortness of breath. Thenurse also explores the patient’s understanding of HF, the self-management strategies, and the desire to adhere to those strate-gies. The nurse helps patients to identify things that they have lostbecause of the diagnosis, their emotional response to that loss, andsuccessful coping skills that they have used previously. Family andsignificant others are often included in these discussions.

PHYSICAL EXAMINATIONThe lungs are auscultated to detect crackles and wheezes or theirabsence. Crackles, which are produced by the sudden opening ofsmall airways and alveoli that have adhered together by edemaand exudate, may be heard at the end of inspiration and are notcleared with coughing. They may also sound like gurgling thatmay clear with coughing or suctioning. The rate and depth of res-pirations are also documented.

The heart is auscultated for an S3 heart sound, a sign that theheart is beginning to fail and that increased blood volume re-mains in the ventricle with each beat. HR and rhythm are alsodocumented. Rapid rates indicate that SV has decreased and thatthe ventricle has less time to fill, producing some blood stagna-tion in the atria and eventually in the pulmonary bed.

JVD is also assessed; distention greater than 3 cm above thesternal angle is considered abnormal. This is an estimate, not aprecise measurement, of central venous pressure.

Sensorium and level of consciousness must be evaluated. Asthe volume of blood ejected by the heart decreases, so does theamount of oxygen transported to the brain.

The nurse makes sure that dependent parts of the patient’sbody are assessed for perfusion and edema. With significant de-creases in SV, there is a decrease in perfusion to the periphery,causing the skin to feel cool and appear pale or cyanotic. If thepatient is sitting upright, the feet and lower legs are examined foredema; if the patient is supine in bed, the sacrum and back areassessed for edema. Fingers and hands may also become edematous.

In extreme cases of HF, the patient may develop periorbital edema,in which the eyelids may swell shut.

The liver is assessed for hepatojugular reflux. The patient isasked to breathe normally while manual pressure is applied overthe right upper quadrant of the abdomen for 30 to 60 seconds. Ifneck vein distention increases more than 1 cm, the test finding ispositive for increased venous pressure.

If the patient is hospitalized, the nurse measures output care-fully to establish a baseline against which to measure the effective-ness of diuretic therapy. Intake and output records are rigorouslymaintained. It is important to know whether the patient hasingested more fluid than he or she has excreted (positive fluidbalance), which is then correlated with a gain in weight. The pa-tient must be monitored for oliguria (diminished urine output,<400 mL/24 hours) or anuria (urine output <50 mL/24 hours).

The patient is weighed daily in the hospital or at home, at thesame time of day, with the same type of clothing, and on thesame scale. If there is a significant change in weight (ie, 2- to 3-lb increase in a day or 5-lb increase in a week), the patient is instructed to notify the physician or adjust the medications(eg, increase the diuretic dose).

DiagnosisNURSING DIAGNOSESBased on the assessment data, major nursing diagnoses for the pa-tient with HF may include the following:

• Activity intolerance (or risk for activity intolerance) relatedto imbalance between oxygen supply and demand becauseof decreased CO

• Excess fluid volume related to excess fluid or sodium intakeand retention of fluid because of HF and its medical therapy

• Anxiety related to breathlessness and restlessness from in-adequate oxygenation

• Powerlessness related to inability to perform role responsi-bilities because of chronic illness and hospitalizations

• Noncompliance related to lack of knowledge

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONSBased on the assessment data, potential complications that maydevelop include the following:

• Cardiogenic shock (see also Chap. 15)• Dysrhythmias (see Chap. 27)• Thromboembolism (see Chap. 31)• Pericardial effusion and cardiac tamponade (see also

Chap. 29)

Planning and GoalsMajor goals for the patient may include promoting activity andreducing fatigue, relieving fluid overload symptoms, decreasingthe incidence of anxiety or increasing the patient’s ability tomanage anxiety, teaching the patient about the self-care pro-gram, and encouraging the patient to verbalize his or her abilityto make decisions and influence outcomes.

Nursing InterventionsPROMOTING ACTIVITY TOLERANCEAlthough prolonged bed rest and even short periods of recumbencypromote diuresis by improving renal perfusion, they also promote


decreased activity tolerance. Prolonged bed rest, which may be self-imposed, should be avoided because of the deconditioning effectsand hazards, such as pressure ulcers (especially in edematous pa-tients), phlebothrombosis, and pulmonary embolism. An acuteevent that causes severe symptoms or that requires hospitaliza-tion indicates the need for initial bed rest. Otherwise, a total of30 minutes of physical activity three to five times each week shouldbe encouraged (Georgiou et al., 2001). The nurse and patient cancollaborate to develop a schedule that promotes pacing and prior-itization of activities. The schedule should alternate activities withperiods of rest and avoid having two significant energy-consumingactivities occur on the same day or in immediate succession.

Before undertaking physical activity, the patient should begiven the following safety guidelines:

• Begin with a few minutes of warm-up activities.• Avoid performing physical activities outside in extreme hot,

cold, or humid weather.• Ensure that you are able to talk during the physical activity;

if you are unable to do so, decrease the intensity of activity.• Wait 2 hours after eating a meal before performing the

physical activity.• Stop the activity if severe shortness of breath, pain, or dizzi-

ness develops.• End with cool-down activities and a cool-down period.

Because some patients may be severely debilitated, they mayneed to perform physical activities only 3 to 5 minutes at a time,one to four times per day. The patient then should be advised toincrease the duration of the activity, then the frequency, beforeincreasing the intensity of the activity (Meyer, 2001).

Barriers to performing an activity are identified, and methodsof adjusting an activity to ensure pacing but still accomplish thetask are discussed. For example, objects that need to be taken up-stairs can be put in a basket at the bottom of the stairs through-out the day. At the end of the day, the person can carry the objectsup the stairs all at once. Likewise, the person can carry cleaningsupplies around in a basket or backpack rather than walk backand forth to obtain the items. Vegetables can be chopped orpeeled while sitting at the kitchen table rather than standing atthe kitchen counter. Small, frequent meals decrease the amountof energy needed for digestion while providing adequate nutri-tion. The nurse helps the patient to identify peak and low peri-ods of energy and plan energy-consuming activities for peakperiods. For example, the person may prepare the meals for theentire day in the morning. Pacing and prioritizing activities helpmaintain the patient’s energy to allow participation in regularphysical activity (see Chap. 28).

The patient’s response to activities needs to be monitored. Ifthe patient is hospitalized, vital signs and oxygen saturationlevel are monitored before, during, and immediately after an ac-tivity to identify whether they are within the desired range.Heart rate should return to baseline within 3 minutes. If the pa-tient is at home, the degree of fatigue felt after the activity canbe used as assessment of the response. If the patient tolerates theactivity, short-term and long-term goals can be developed togradually increase the intensity, duration, and frequency of ac-tivity. Referral to a cardiac rehabilitation program may be needed,especially for HF patients with recent myocardial infarction, recent open-heart surgery, or increased anxiety. A supervised pro-gram may also benefit those who need the structured environ-ment, significant educational support, regular encouragement,and interpersonal contact.

MANAGING FLUID VOLUMEPatients with severe HF may receive intravenous diuretic therapy,but patients with less severe symptoms may receive oral diureticmedication (see Table 30-4 for a summary of common diuretics).Oral diuretics should be administered early in the morning sothat diuresis does not interfere with the patient’s nighttime rest.Discussing the timing of medication administration is especiallyimportant for patients, such as elderly people, who may have uri-nary urgency or incontinence. A single dose of a diuretic maycause the patient to excrete a large volume of fluid shortly afteradministration.

The nurse monitors the patient’s fluid status closely—auscultating the lungs, monitoring daily body weights, and as-sisting the patient to adhere to a low-sodium diet by reading foodlabels and avoiding high-sodium foods such as canned, processed,and convenience foods (Chart 30-4). If the diet includes fluid re-striction, the nurse can assist the patient to plan the fluid in-take throughout the day while respecting the patient’s dietarypreferences. If the patient is receiving intravenous fluids, the

Facts About Dietary Sodium

Although the major source of sodium in the average Americandiet is salt, many types of natural foods contain varying amountsof sodium. Even if no salt is added in cooking and if salty foodsare avoided, the daily diet may still contain between 1000 and2000 mg of sodium.

Additives in FoodAdded food substances (additives), such as sodium alginate, whichimproves food texture; sodium benzoate, which acts as a preserv-ative; and disodium phosphate, which improves cooking qualityin certain foods, increase the sodium intake when included in thedaily diet. Therefore, patients on low-sodium diets should be ad-vised to check labels carefully for such words as “salt” or “sodium,”especially on canned foods. For example, without looking at thesodium content per serving found on the nutrition labels, whengiven a choice between a serving of salt and vinegar potato chipsand a cup of canned cream of mushroom soup, most would thinkthat soup is lower in sodium. However, when the labels are exam-ined, the lower sodium choice is found to be the chips. Althoughpotato chips are not recommended in a low sodium diet, this ex-ample illustrates that it is important to read food labels to deter-mine both sodium content and serving size.

Nonfood Sodium SourcesSodium is also contained in toothpaste and municipal water. Patientson sodium-restricted diets should be cautioned against using non-prescription medications such as antacids, cough syrups, laxatives,sedatives, or salt substitutes, because these products contain sodiumor excessive amounts of potassium. Over-the-counter medicationsshould not be used without first consulting the physician.

Promoting Dietary AdherenceIf patients find food unpalatable because of the dietary sodium re-strictions and/or the taste disturbances caused by the medications,they may refuse to eat or to comply with the dietary regimen. Forthis reason, severe sodium restrictions should be avoided and theamount of medication should be balanced with the patient’s abil-ity to restrict dietary sodium. A variety of flavorings, such as lemonjuice, vinegar, and herbs, may be used to improve the taste of thefood and increase acceptance of the diet. The patient’s food prefer-ences should be taken into account—diet counseling and educa-tional handouts can be geared to individual and ethnic preferences.It is very important to involve the family in the dietary teaching.

Chart30-4

Chart30-4


amount of fluid needs to be monitored closely, and the physi-cian or pharmacist can be consulted about the possibility ofmaximizing the amount of medication in the same amount ofintravenous fluid (eg, double-concentrating to decrease thefluid volume administered).

The nurse positions the patient or teaches the patient how toassume a position that shifts fluid away from the heart. The num-ber of pillows may be increased, the head of the bed may be elevated (20- to 30-cm [8- to 10-inch] blocks may be used), orthe patient may sit in a comfortable armchair. In this position, thevenous return to the heart (preload) is reduced, pulmonary con-gestion is alleviated, and impingement of the liver on the di-aphragm is minimized. The lower arms are supported with pillowsto eliminate the fatigue caused by the constant pull of theirweight on the shoulder muscles.

The patient who can breathe only in the upright position maysit on the side of the bed with the feet supported on a chair, thehead and arms resting on an overbed table, and the lumbosacralspine supported by a pillow. If pulmonary congestion is present,positioning the patient in an armchair is advantageous, becausethis position favors the shift of fluid away from the lungs.

Because decreased circulation in edematous areas increases therisk of skin injury, the nurse assesses for skin breakdown and in-stitutes preventive measures. Frequent changes of position, posi-tioning to avoid pressure, the use of elastic compression stockings,and leg exercises may help to prevent skin injury.

CONTROLLING ANXIETYBecause patients in HF have difficulty maintaining adequate oxy-genation, they are likely to be restless and anxious and feel over-whelmed by breathlessness. These symptoms tend to intensify atnight. Emotional stress stimulates the sympathetic nervous sys-tem, which causes vasoconstriction, elevated arterial pressure, andincreased heart rate. This sympathetic response increases theamount of work that the heart has to do. By decreasing anxiety,the patient’s cardiac work also is decreased. Oxygen may be ad-ministered during an acute event to diminish the work of breath-ing and to increase the patient’s comfort.

When the patient exhibits anxiety, the nurse takes steps topromote physical comfort and psychological support. In manycases, a family member’s presence provides reassurance. To helpdecrease the patient’s anxiety, the nurse should speak in a slow,calm, and confident manner and maintain eye contact. Whennecessary, the nurse should also state specific, brief directions foran activity.

After the patient is comfortable, the nurse can begin teachingways to control anxiety and to avoid anxiety-provoking situa-tions. The nurse explains how to use relaxation techniques andassists the patient to identify factors that contribute to anxiety.Lack of sleep may increase anxiety, which may prevent adequaterest. Other contributing factors may include misinformation,lack of information, or poor nutritional status. Promoting phys-ical comfort, providing accurate information, and teaching thepatient to perform relaxation techniques and to avoid anxiety-triggering situations may relax the patient.

In cases of confusion and anxiety reactions that affect the pa-tient’s safety, the use of restraints should be avoided. Restraintsare likely to be resisted, and resistance inevitably increases the car-diac workload. The patient who insists on getting out of bed atnight can be seated comfortably in an armchair. As cerebral andsystemic circulation improves, the degree of anxiety decreases,and the quality of sleep improves.

MINIMIZING POWERLESSNESSPatients need to recognize that they are not helpless and that theycan influence the direction of their lives and the outcomes oftreatment. The nurse assesses for factors contributing to a senseof powerlessness and intervenes accordingly. Contributing factorsmay include lack of knowledge and lack of opportunities to makedecisions, particularly if health care providers and family mem-bers behave in maternalistic or paternalistic ways. If the patient ishospitalized, hospital policies may promote standardization andlimit the patient’s ability to make decisions (eg, what time to havemeals, take medications, prepare for bed).

Taking time to listen actively to patients often encourages themto express their concerns and ask questions. Other strategies in-clude providing the patient with decision-making opportunities,such as when activities are to occur or where objects are to beplaced, and increasing the frequency and significance of those op-portunities over time; providing encouragement while identifyingthe patient’s progress; and assisting the patient to differentiate be-tween factors that can be controlled and those that cannot. In somecases, the nurse may want to review hospital policies and standardsthat tend to promote powerlessness and advocate for their elimi-nation or change (eg, limited visiting hours, prohibition of foodfrom home, required wearing of hospital gowns).

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-CareThe nurse provides patient education and involves the patient inimplementing the therapeutic regimen to promote understand-ing and adherence to the plan. When the patient understands orbelieves that the diagnosis of HF can be successfully managedwith lifestyle changes and medications, recurrences of acute HFlessen, unnecessary hospitalizations decrease, and life expectancyincreases. Patients and their families need to be taught to followthe medication regimen as prescribed, maintain a low-sodiumdiet, perform and record daily weights, engage in routine physi-cal activity, and recognize symptoms that indicate worsening HF.Although noncompliance is not well understood, interventionsthat may promote adherence include teaching to ensure accurateunderstanding. A summary of teaching points for the patientwith HF is presented in Chart 30-5.

The patient and family members are supported and encouragedto ask questions so that information can be clarified and under-standing enhanced. The nurse should be aware of cultural factorsand adapt the teaching plan accordingly. Patients and their fami-lies need to be informed that the progression of the disease is in-fluenced in part by choices made about health care and thedecisions about following the treatment plan. They also need to beinformed that health care providers are there to assist them inreaching their health care goals. Patients and family members needto make the decisions about the treatment plan, but they also needto understand the possible outcomes of those decisions. The treat-ment plan then will be based on what the patient wants, not justwhat the physician or other health care team members think isneeded. Ultimately, the nurse needs to convey that monitoringsymptoms and daily weights, restricting sodium intake, avoiding

NURSING ALERT Cerebral hypoxia with superimposed carbondioxide retention may be a problem in HF, causing the patient toreact to sedative-hypnotic medications with confusion and increasedanxiety. Hepatic congestion may slow the liver’s metabolism ofmedication, leading to toxicity. Sedative-hypnotic medicationsmust be administered with caution.

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excess fluids, preventing infection with influenza and pneumococ-cal immunizations, avoiding noxious agents (eg, alcohol, tobacco),and participating in regular exercise all aid in preventing exacerba-tions of HF.

Continuing CareDepending on the patient’s physical status and the availabilityof family assistance, a home care referral may be indicated for apatient who has been hospitalized. Elderly patients and thosewho have long-standing heart disease with compromised phys-ical stamina often require assistance with the transition to homeafter hospitalization for an acute episode of HF. It is importantfor the home care nurse to assess the physical environment ofthe home. Suggestions for adapting the home environment tomeet the patient’s activity limitations are important. If stairs arethe concern, the patient can plan the day’s activities so that stairclimbing is minimized; for some patients, a temporary bedroommay be set up on the main level of the home. The home carenurse collaborates with the patient and family to maximize thebenefits of these changes.

The home care nurse also reinforces and clarifies informationabout dietary changes and fluid restrictions, the need to monitorsymptoms and daily body weights, and the importance of obtain-ing follow-up health care. Assistance may be given in schedulingand keeping appointments as well. The patient is encouraged togradually increase his or her self-care and responsibility for ac-complishing the therapeutic regimen.

EvaluationEXPECTED PATIENT OUTCOMESExpected patient outcomes may include:

1. Demonstrates tolerance for increased activitya. Describes adaptive methods for usual activitiesb. Stops any activity that causes symptoms of intolerancec. Maintains vital signs (pulse, blood pressure, respira-

tory rate, and pulse oximetry) within the targetedrange

d. Identifies factors that contribute to activity intoleranceand takes actions to avoid them

e. Establishes priorities for activitiesf. Schedules activities to conserve energy and to reduce

fatigue and dyspnea2. Maintains fluid balance

a. Exhibits decreased peripheral and sacral edemab. Demonstrates methods for preventing edema

3. Is less anxiousa. Avoids situations that produce stressb. Sleeps comfortably at nightc. Reports decreased stress and anxiety

4. Makes decisions regarding care and treatmenta. States ability to influence outcomes

5. Adheres to self-care regimena. Performs and records daily weightsb. Ensures dietary intake includes no more than 2 to 3 g

of sodium per day

Chart 30-5Home Care Checklist • The Patient With Heart Failure

At the completion of the home care instruction, the patient or caregiver will be able to:

• Identify heart failure as a chronic disease that can be managed with medications and specific self-management behaviors. ✓ ✓

• Take or administer medications daily, exactly as prescribed. ✓ ✓

• Monitor effects of medication. ✓ ✓

• Know signs and symptoms of orthostatic hypotension and how to prevent it. ✓ ✓

• Weigh self daily. ✓

– Obtain weight at the same time each day (eg, every morning after urination).– Keep a record and report weight gain of ≥ 2–3 lb (0.9–1.4 kg) in 1 day or 5 lb (2.3 kg) in 1 week.

• Restrict sodium intake to 2–3 g daily: adapt diet by examining nutrition labels to check sodium content per serving; avoid canned or processed foods; eat fresh or frozen foods; consult the written diet plan and the list of permitted and restricted foods; avoid salt use; and avoid excesses in eating and drinking. ✓ ✓

• Review activity program. ✓– Participate in a daily exercise program.– Increase walking and other activities gradually, provided they do not cause unusual fatigue or dyspnea.– Conserve energies by balancing activity with rest periods.– Avoid activity in extremes of heat and cold, which increase the work of the heart.– Recognize that air conditioning may be essential in a hot, humid environment.

• Develop methods to manage stress. ✓

• Keep regular appointments with physician or clinic. ✓ ✓

• Be alert for symptoms that may indicate recurring heart failure. ✓ ✓– Recall the symptoms experienced when illness began.

• Report immediately to the physician or clinic any of the following: ✓ ✓– Gain in weight of ≥ 2–3 lb (0.9–1.4 kg) in 1 day, or 5 lb (2.3 kg) in 1 week– Loss of appetite– Unusual shortness of breath with activity– Swelling of ankles, feet, or abdomen– Persistent cough– Development of restless sleep; increase in number of pillows needed to sleep

Patient Caregiver


c. Takes medications as prescribedd. Reports any unusual symptoms or side effects

ACUTE HEART FAILURE (PULMONARY EDEMA)Pulmonary edema is the abnormal accumulation of fluid in thelungs. The fluid may accumulate in the interstitial spaces or inthe alveoli.

PathophysiologyPulmonary edema is an acute event that results from HF. It canoccur acutely, such as with myocardial infarction, or it canoccur as an exacerbation of chronic HF. Myocardial scarring asa result of ischemia can limit the ventricular distensibility andrender it vulnerable to a sudden increase in workload. With in-creased resistance to left ventricular filling, the blood backs upinto the pulmonary circulation. The patient quickly developspulmonary edema, sometimes called flash pulmonary edema,from the blood volume overload in the lungs. Pulmonaryedema can also be caused by noncardiac disorders, such as renalfailure, liver failure, and oncologic conditions that cause thebody to retain fluid. The left ventricle cannot handle the re-sulting hypervolemia, preventing blood from easily flowingfrom the left atrium into the left ventricle. This causes the pres-sure to increase in the left atrium. The increase in atrial pres-sure may result in an increase in pulmonary venous pressure,which produces an increase in hydrostatic pressure that forcesfluid out of the pulmonary capillaries into the interstitial spacesand alveoli.

Impaired lymphatic drainage also contributes to the accumu-lation of fluid in the lung tissues. The fluid within the alveolimixes with air, creating “bubbles” that are expelled from themouth and nose, producing the classic symptom of pulmonaryedema, frothy pink (blood-tinged) sputum. Because of the fluidwithin the alveoli, air cannot enter, and gas exchange is impaired.The result is hypoxemia, which is often severe. The onset may bepreceded by premonitory symptoms of pulmonary congestion,but it also may develop quickly in the patient with a ventricle thathas little reserve to meet increased oxygen needs.

In pulmonary edema, as well as in HF, preload, contractility,and afterload may be altered, thereby impairing CO. Techno-logical advances (eg, impedance cardiography) have made it eas-ier to implement effective pharmacologic therapy in treatingacute pulmonary edema.

Clinical ManifestationsAs a result of decreased cerebral oxygenation, the patient be-comes increasingly restless and anxious. Along with a suddenonset of breathlessness and a sense of suffocation, the patient’shands become cold and moist, the nail beds become cyanotic(bluish), and the skin turns ashen (gray). The pulse is weak andrapid, and the neck veins are distended. Incessant coughing mayoccur, producing increasing quantities of mucoid sputum. Aspulmonary edema progresses, the patient’s anxiety and restless-ness increase; the patient becomes confused, then stuporous.Breathing is rapid, noisy, and moist sounding. The patient’soxygen levels (saturation) are significantly decreased. The pa-tient, nearly suffocated by the blood-tinged, frothy fluid fillingthe alveoli, is literally drowning in secretions. The situation de-mands immediate action.

Assessment and Diagnostic FindingsThe diagnosis is made by evaluating the clinical manifestations re-sulting from pulmonary congestion. Most often, a chest x-ray is ob-tained to confirm that the pulmonary veins are engorged. Abruptonset of signs and symptoms of left-sided HF(eg, crackles on aus-cultation of the lungs, flash pulmonary edema) without evidenceof right-sided HF (eg, no JVD, no dependent edema) may indicatediastolic failure due to ischemia.

PreventionLike most complications, pulmonary edema is easier to preventthan to treat. To recognize it in its early stages, the nurse aus-cultates the lung fields and heart sounds, measures JVD, andassesses the degree of peripheral edema and the severity of breath-lessness. A dry, hacking cough; fatigue; weight gain; developmentor worsening of edema; and decreased activity tolerance may beearly indicators of developing pulmonary edema.

In an early stage, the condition may be corrected by placingthe patient in an upright position with the feet and legs depen-dent, eliminating overexertion, and minimizing emotional stressto reduce the left ventricular load. A re-examination of the pa-tient’s treatment regimen and the patient’s understanding of andadherence to it are also needed. The long-range approach to pre-venting pulmonary edema must be directed at identifying itsprecipitating factors.

Medical ManagementClinical management of a patient with acute pulmonary edemadue to HF is directed toward improving ventricular function andincreasing respiratory exchange. These goals are accomplishedthrough a combination of oxygen, medication therapies, andnursing support.

PHARMACOLOGIC THERAPYVarious treatments and medications are prescribed for pul-monary edema, among them oxygen, morphine, diuretics, andvarious intravenous medications.

Oxygen Therapy. Oxygen is administered in concentrations ad-equate to relieve hypoxemia and dyspnea. Usually, a face maskor non-rebreathing mask is initially used. If respiratory failureis severe or persists despite optimal management, endotrachealintubation and mechanical ventilation are required. The use ofpositive end-expiratory pressure (PEEP) is effective in reducingvenous return, decreasing fluid movement from the pulmonarycapillaries to the alveoli, and improving oxygenation. Oxy-genation is monitored with pulse oximetry and by measurementof arterial blood gases.

Morphine. Morphine is administered intravenously in small doses(2 to 5 mg) to reduce peripheral resistance and venous return sothat blood can be redistributed from the pulmonary circulation toother parts of the body. This action decreases pressure in the pul-monary capillaries and decreases seepage of fluid into the lung tis-sue. The effect of morphine in decreasing anxiety is also beneficial.

Diuretics. Diuretics promote the excretion of sodium and waterby the kidneys. Furosemide (Lasix), for example, is administeredintravenously to produce a rapid diuretic effect. Furosemide alsocauses vasodilation and pooling of blood in peripheral blood


vessels, which reduces the amount of blood returned to the heart,even before the diuretic effect. Some physicians may prescribebumetanide (Bumex) and metolazone (Mykrox, Zaroxolyn) inplace of furosemide.

Dobutamine. Dobutamine (Dobutrex) is an intravenous medica-tion given to patients with significant left ventricular dysfunction.A catecholamine, dobutamine stimulates the beta1-adrenergicreceptors. Its major action is to increase cardiac contractility.However, at higher amounts, it also increases the heart rate andthe incidence of ectopic beats and tachydysrhythmias. Becauseit also increases AV conduction, care must be taken in patientswho have underlying atrial fibrillation. A medication that pro-tects the AV node, such as digitalis, a beta-blocker, or a calciumchannel blocker, may be indicated before dobutamine therapyis initiated to prevent increased ventricular response rate.

Milrinone. Milrinone (Primacor) is a phosphodiesterase in-hibitor that delays the release of calcium from intracellular reser-voirs and prevents the uptake of extracellular calcium by the cells.This promotes vasodilation, decreasing preload and afterload, re-ducing the workload of the heart. Milrinone is administered in-travenously, usually to patients who have not responded to othertherapies. It is not usually used to treat patients with renal failure.The major side effects are hypotension (usually asymptomatic),gastrointestinal dysfunction, increased ventricular dysrhythmias,and decreased platelet counts. The patient’s blood pressure ismonitored closely.

Nesiritide. Nesiritide (Natrecor) is an intravenous medicationthat is indicated for acutely decompensated HF. Natriuretic pep-tides are produced by the myocardium as a compensatory re-sponse to increased ventricular end-diastolic pressure andmyocardial wall stress and to the increased release of neuro-hormones (eg, norepinephrine, renin, aldosterone) that occurwith HF. Nesiritide is a human B-type natriuretic peptide (BNP)made from Escherichia coli using recombinant technology. HumanBNP binds to vascular smooth muscle and endothelial cells,causing dilation of arteries and veins and suppression of the neu-rohormones. The result is improved stroke volume and reducedpreload and afterload (Colucci et al., 2000). This medicationcauses rapid improvement in the symptoms of HF and may beused with other HF medications (eg, beta-blockers, digoxin). Themost common side effect is dose-related hypotension.

Nursing ManagementPOSITIONING THE PATIENT TO PROMOTE CIRCULATIONProper positioning can help reduce venous return to the heart.The patient is positioned upright, preferably with the legs dan-gling over the side of the bed. This has the immediate effect ofdecreasing venous return, lowering the output of the right ven-tricle, and decreasing lung congestion. If the patient is unable tosit with the lower extremities dependent, the patient may beplaced in an upright position in bed.

PROVIDING PSYCHOLOGICAL SUPPORTAs the ability to breathe decreases, the patient’s sense of fear andanxiety rises proportionately, making the condition more severe.Reassuring the patient and providing skillful anticipatory nursingcare are integral parts of the therapy. Because this patient feels asense of impending doom and has an unstable condition, thenurse must remain with the patient. The nurse should give the pa-

tient simple, concise information in a reassuring voice about whatis being done to treat the condition and the expected results. Thenurse should also identify any anxiety-inducing factors (eg, a petleft alone at home, presence of an unwelcome family member atthe bedside, a wallet full of money) and initiate strategies to elim-inate the concern or reduce its effect.

MONITORING MEDICATIONSThe patient receiving morphine is observed for respiratory de-pression, hypotension, and vomiting; a morphine antagonist,such as naloxone hydrochloride (Narcan), is kept available andgiven to the patient who exhibits these side effects.

The patient receiving diuretic therapy may excrete a large vol-ume of urine within minutes after a potent diuretic is adminis-tered. A bedside commode may be used to decrease the energyrequired by the patient and to reduce the resultant increase in car-diac workload induced by getting on and off a bedpan. If neces-sary, an indwelling urinary catheter may be inserted.

Other ComplicationsCARDIOGENIC SHOCKCardiogenic shock occurs when the heart cannot pump enoughblood to supply the amount of oxygen needed by the tissues.This may occur because of one significant or multiple smallerinfarctions in which more than 40% of the myocardium be-comes necrotic, because of a ruptured ventricle, significantvalvular dysfunction, trauma to the heart resulting in myocar-dial contusion, or as the end stage of HF. It also can occur withcardiac tamponade, pulmonary embolism, cardiomyopathy,and dysrhythmias.

PathophysiologyThe signs and symptoms of cardiogenic shock reflect the circularnature of the pathophysiology of HF. The degree of shock is pro-portional to the extent of left ventricular dysfunction. The heartmuscle loses its contractile power, resulting in a marked reduc-tion in SV and CO, which is sometimes called forward failure.The damage to the myocardium results in a decrease in CO,which reduces arterial blood pressure and tissue perfusion in thevital organs (heart, brain, lung, kidneys). Flow to the coronaryarteries is reduced, resulting in decreased oxygen supply to themyocardium, which increases ischemia and further reduces theheart’s ability to pump. The inadequate emptying of the ven-tricle also leads to increased pulmonary pressures, pulmonarycongestion, and pulmonary edema, exacerbating the hypoxia,causing ischemia of vital organs, and setting a vicious cycle inmotion (Fig. 30-3).

NURSING ALERT Because of the resulting diuresis, the patient’selectrolyte levels, especially potassium and sodium, need to bemonitored closely. Fluid balance in some patients is very brittle;they easily become hypovolemic or hypervolemic with smallchanges in the amount of circulating fluid. Falling blood pressure,increasing heart rate, and decreasing urine output indicate that thecirculatory system is not tolerating diuresis and that measures mustbe taken to reverse the fluid imbalance that has occurred. Serumcreatinine is monitored to assess renal function. Men with prostatichyperplasia must be observed for signs of urinary retention. Additional monitoring activities are discussed in Chart 30-6.

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Chart 30-6 • PHARMACOLOGYAdministering and Monitoring Diuretic Therapy

When nursing care involves diuretic therapy for conditions such aspulmonary edema or heart failure, the nurse needs to administer themedication and monitor the patient’s response carefully, as follows:

• Administer the diuretic at a time conducive to the patient’slifestyle; for example, early in the day to avoid nocturia.

• Give supplementary potassium with thiazide and loop diuretics as prescribed to replace potassium lost.

• Check laboratory results for electrolyte depletion, especiallypotassium, magnesium, and sodium; and for electrolyte ele-vation, especially potassium with potassium-sparing agentsand calcium with thiazides.

• Monitor urine output or daily weights to identify appro-priate response: intake and output balance, serum BUNand creatinine; notify the health care provider if renal impairment is suspected.

• Assess lung sounds, jugular vein distention, daily weight,and peripheral, abdominal, or sacral edema to identifyneed to adjust dose.

• Monitor for adverse reactions, such as nausea and gastrointesti-nal distress, vomiting, diarrhea, weakness, headache, fatigue,anxiety or agitation, and cardiac dysrhythmias.

• Assess for signs of volume depletion, such as posturalhypotension, dizziness, imbalance, and reduced jugular venous distention (JVD).

• Monitor for glucose intolerance in patients with and with-out diabetes mellitus who are receiving thiazide diuretics.

• Monitor for potential ototoxicity in patients, especially thosewith renal failure, who are receiving a loop diuretic.

• Advise patients to avoid prolonged exposure to the sun because of the risk of photosensitivity.

• Monitor for elevated serum uric acid levels and the develop-ment of gout.

• Implement nursing actions to facilitate effect of medication,such as positioning patient upright with legs dangling.

Clinical ManifestationsThe classic signs of cardiogenic shock are tissue hypoperfusionmanifested as cerebral hypoxia (restlessness, confusion, agitation),low blood pressure, rapid and weak pulse, cold and clammy skin,increased respiratory crackles, hypoactive bowel sounds, and de-creased urinary output. Initially, arterial blood gas analysis mayshow respiratory alkalosis. Dysrhythmias are common and resultfrom a decrease in oxygen to the myocardium.

Assessment and Diagnostic FindingsUse of a PA catheter to measure left ventricular pressures and COis important in assessing the severity of the problem and planningmanagement. The PA wedge pressure is elevated and the CO de-creased as the left ventricle loses its ability to pump. The systemicvascular resistance is elevated because of the sympathetic nervoussystem stimulation that occurs as a compensatory response to thedecrease in blood pressure. The decreased blood flow to the kid-neys causes a hormonal response (ie, increased catecholaminesand activation of the renin-angiotensin-aldosterone system) thatcauses fluid retention and further vasoconstriction. Increases inHR, circulating volume, and vasoconstriction occur to maintaincirculation to the brain, heart, kidneys, and lungs, but at a cost:an increase in the workload of the heart.

The reduction in blood volume delivered to the tissues resultsin an increase in the amount of oxygen that is extracted from theblood that is delivered to the tissues (to try to meet the cellular de-mand for oxygen). The increased systemic oxygen extraction resultsin decreased venous (mixed and central) oxygen saturation. Whenthe cellular oxygen needs cannot be met by the systemic oxygendelivery and the oxygen extraction, anaerobic metabolism and theresulting build up of lactic acid occur. Continuous central venousoximetry and measurement of blood lactic acid levels may assistin assessing the severity of the shock as well as the effectiveness oftreatment.

Continued cellular hypoperfusion eventually results in organfailure. The patient becomes unresponsive, severe hypotensionensues, and the patient develops shallow respirations; cold, cya-notic or mottled skin; and absent bowel sounds. Arterial bloodgas analysis shows metabolic acidosis, and all laboratory test resultsindicate organ dysfunction. Chapter 15 presents in more detail thepathophysiology and management of cardiogenic shock.

Medical ManagementThe major approach to treating cardiogenic shock is to correct theunderlying problems, reduce any further demand on the heart, im-prove oxygenation, and restore tissue perfusion. For example, if theventricular failure is the result of an acute myocardial infarction,emergency percutaneous coronary intervention may be indicated(Webb et al., 2001). Ventricular assist devices may be implantedto support the pumping action of the heart (Barron et al., 2001)(see Chap. 29). Major dysrhythmias are corrected because theymay have caused or contributed to the shock. If the patient hashypervolemia, diuresis is indicated. Diuretics, vasodilators, and me-chanical devices, such as filtration (continuous renal replacementtherapy [CRRT]) and dialysis, have been used to reduce the circu-lating blood volume. If hypovolemia or low intravascular volumeis suspected or detected through pressure readings, the patient isgiven intravenous volume expanders (eg, normal saline solution,lactated Ringer’s solution, albumin) to increase the amount of cir-culating fluid. The patient is placed on strict bedrest to conserve

FIGURE 30-3 Pathophysiology of cardiogenic shock.

Decreased contractility

Myocardial ischemia

Hypoxia

Increased pulmonary pressure

Increased pulmonary blood volume

Decreased coronary artery perfusion

Decreased blood pressure

Decreased cardiac output

Physiology/Pathophysiology


energy. If the patient has hypoxemia, as detected by pulse oxime-try or arterial blood gas analysis, oxygen administration is increased,often under positive pressure when regular flow is insufficient tomeet tissue demands. Intubation and sedation may be necessaryto maintain oxygenation. The settings for mechanical ventilationare adjusted according to the patient’s oxygenation status and theneed for conserving energy.

PHARMACOLOGIC THERAPYMedication therapy is selected and guided according to CO, othercardiac parameters, and mean arterial blood pressure. Because ofthe decreased perfusion to the gastrointestinal system and the needto adjust the dosage quickly, most medications are administeredintravenously.

Vasopressors, or pressor agents, are medications used to raiseblood pressure and increase CO. Many pressor medications arecatecholamines, such as norepinephrine (Levophed) and high-dose (>10 µg/kg per minute) dopamine (Intropin). Their pur-pose is to promote perfusion to the heart and brain, but theycompromise circulation to other organs (eg, kidney). Becausethey also tend to increase the workload of the heart by increasingoxygen demand, they are not administered early in the cardio-genic shock process.

Diuretics and vasodilators may be administered carefully toreduce the workload of the heart as long as they do not causeworsening of the tissue hypoperfusion. Agents such as amrinone(Inocor), milrinone (Primacor), sodium nitroprusside (Nipride),and nitroglycerin (Tridil) are effective vasoactive medicationsthat lower the volume returning to the heart, decrease bloodpressure, and decrease cardiac work. They cause the arteries andveins to dilate, thereby shunting much of the intravascular volume to the periphery and causing a reduction in preload andafterload.

Positive inotropic medications are given to increase myocardialcontractility. Dopamine (Intropin, given at more than 2 µg/kg perminute), dobutamine (Dobutrex), and epinephrine (Adrenalin)are catecholamines that increase contractility. Each of these cancause tachydysrhythmias because they increase automaticity withincreasing dosage. Monitoring baseline HR is therefore impor-tant. As the baseline HR increases, so does the risk of developingtachydysrhythmias.

OTHER TREATMENTSOther therapeutic modalities for cardiogenic shock include use ofcirculatory assist devices. The most frequently used mechanicalsupport device is the intra-aortic balloon pump (IABP). The IABPis a catheter with an inflatable balloon at the end. The catheter isusually inserted through the femoral artery, and the balloon is po-sitioned in the descending thoracic aorta (Fig. 30-4). IABP usesinternal counterpulsation through the regular inflation and defla-tion of the balloon to augment the pumping action of the heart.The device inflates during diastole, increasing the pressure in theaorta during diastole and therefore increasing blood flow throughthe coronary and peripheral arteries. It deflates just before systole,lessening the pressure within the aorta before left ventricular con-traction, decreasing the amount of resistance the heart has to over-come to eject blood and therefore decreasing the amount of workthe heart must put forth to eject blood. The device is connectedto a console that synchronizes the inflation and deflation of theballoon with the ECG or the arterial pressure (as indicators for sys-tole and diastole). Hemodynamic monitoring is essential to de-termine the patient’s response to the IABP. Other ventricularassist devices are described in Chapter 29.

Nursing ManagementThe patient in cardiogenic shock requires constant monitoringand intensive care. The critical care (intensive care) nurse mustcarefully assess the patient, observe the cardiac rhythm, monitorhemodynamic parameters, and record fluid intake and urinaryoutput. The patient must be closely assessed for responses to themedical interventions and for the development of complications,which must be corrected immediately.

Because of the frequency of nursing interventions and thetechnology required for effective medical management, the pa-tient is always treated in an intensive care environment. Criticalcare nurses are responsible for the nursing management, whichincludes frequent assessments and timely adjustments to medica-tions and therapies based on the assessment data. More informa-tion about nursing management of the patient in cardiogenicshock can be found in Chapter 15.

THROMBOEMBOLISMThe decreased mobility of the patient with cardiac disease and theimpaired circulation that accompany these disorders contributeto the development of intracardiac and intravascular thrombosis.Intracardiac thrombus is especially common in patients withatrial fibrillation, because the atria do not contract forcefully

Diastole Systole

FIGURE 30-4 The intra-aortic balloon pump (IABP) inflates at the be-ginning of diastole, which results in increased perfusion of the coronary andperipheral arteries; it deflates just before systole, which results in a decreasein afterload (resistance to ejection) and in the left ventricular workload.


and blood flow slows through the atrium, increasing thrombus for-mation. Intracardiac thrombus is detected by an echocardiogramand treated with anticoagulants, such as heparin and warfarin(Coumadin). A part of the thrombus may become detached (embolus) and may be carried to the brain, kidneys, intestines,or lungs. The most common problem is pulmonary embolism.The symptoms of pulmonary embolism include chest pain,cyanosis, shortness of breath, rapid respirations, and hemoptysis(bloody sputum).

The pulmonary embolus may block the circulation to a part ofthe lung, producing an area of pulmonary infarction. Usually, thereis a significant decrease in oxygenation measured by arterial bloodgas analysis or pulse oximetry. Pain experienced is usually pleuritic;it increases with respiration and may subside when the patientholds the breath. Cardiac pain is usually continuous and does notvary with respirations. However, it may be difficult to differentiateby symptoms alone. The patient usually undergoes a ventilation-perfusion scan or a pulmonary arteriogram for definitive diagnosis.The treatment and care for patients with pulmonary embolism arediscussed in Chapter 23.

Systemic embolism may manifest as cerebral, mesenteric, orrenal infarction; an embolism can also compromise the bloodsupply to an extremity, which is discussed in more detail in Chap-ter 31. The nurse must be aware of such possible complicationsand be prepared to identify and report signs and symptoms.

PERICARDIAL EFFUSION AND CARDIAC TAMPONADEPathophysiologyPericardial effusion refers to the accumulation of fluid in the peri-cardial sac. This occurrence may accompany pericarditis (seeChap. 29), advanced HF, metastatic carcinoma, cardiac surgery,trauma, or nontraumatic hemorrhage.

Normally, the pericardial sac contains less than 50 mL of fluid,which is needed to decrease friction for the beating heart. An in-crease in pericardial fluid raises the pressure within the pericardialsac and compresses the heart. This has the following effects:

• Increased right and left ventricular end-diastolic pressures• Decreased venous return• Inability of the ventricles to distend adequately and to fill

Pericardial fluid may accumulate slowly without causing no-ticeable symptoms. A rapidly developing effusion, however, canstretch the pericardium to its maximum size and, because of in-creased pericardial pressure, reduce venous return to the heart anddecrease CO. The result is cardiac tamponade (compression ofthe heart).

Clinical ManifestationsThe patient may complain of a feeling of fullness within the chestor may have substantial or ill-defined pain. The feeling of pres-sure in the chest may result from stretching of the pericardial sac.Because of increased pressure within the pericardium, venouspressure tends to rise, as evidenced by engorged neck veins. Othersigns include shortness of breath and a drop and fluctuation inblood pressure. Systolic blood pressure that is detected during ex-halation but not heard with inhalation is called pulsus para-doxus. The difference in systolic pressure between the point thatit is heard during exhalation and the point that it is heard duringinhalation is measured. Pulsus paradoxus exceeding 10 mm Hg

is abnormal. The cardinal signs of cardiac tamponade are fallingsystolic blood pressure, narrowing pulse pressure, rising venouspressure (increased jugular venous distention), and distant (muf-fled) heart sounds (Chart 30-7).

Assessment and Diagnostic FindingsPericardial effusion is detected by percussing the chest and notic-ing an extension of flatness across the anterior aspect of the chest.An echocardiogram may be performed to confirm the diagnosis.The clinical signs and symptoms and chest x-ray findings are usu-ally sufficient to diagnose pericardial effusion.

Medical ManagementPERICARDIOCENTESISIf cardiac function becomes seriously impaired, pericardiocen-tesis (puncture of the pericardial sac to aspirate pericardial fluid)is performed to remove fluid from the pericardial sac. The major

NURSING ALERT Cardiac tamponade is a life-threatening situation, demanding immediate intervention.!

Chart 30-7 • ASSESSMENT

Signs and Symptoms of Cardiac Tamponade

Assessment findings in cardiac tamponade resulting from pericardialeffusion include feelings of faintness, shortness of breath, anxiety, andpain from decreased cardiac output, cough from pressure createdin the trachea from swelling of the pericardial sac, distended neckveins from rising venous pressure, paradoxical pulse, and muffledor distant heart sounds.

Rising venous pressureFalling arterial pressureQuiet heart sounds

Dyspnea and decreasedcardiac output

Paradoxical pulse

Syncope, anxiety

Prominent neckveins due to elevated venouspressure

Precordial compressiondue to stretching of

pericardial sac; coughdue to compression of

trachea and bronchiby expanding

pericardial sac

Muffledheart sounds


goal is to prevent cardiac tamponade, which restricts normal heartaction.

During the procedure, the patient is monitored by ECG andhemodynamic pressure measurements. Emergency resuscitativeequipment should be readily available. The head of the bed is el-evated to 45 to 60 degrees, placing the heart in proximity to thechest wall so that the needle can be inserted into the pericardialsac more easily. If a peripheral intravenous device is not alreadyin place, one is inserted, and a slow intravenous infusion is startedin case it becomes necessary to administer emergency medicationsor blood products.

The pericardial aspiration needle is attached to a 50-mL sy-ringe by a three-way stopcock. Several possible sites are used forpericardial aspiration. The needle may be inserted in the angle be-tween the left costal margin and the xiphoid, near the cardiacapex; at the fifth or sixth intercostal space at the left sternal mar-gin; or on the right sternal margin of the fourth intercostal space.The needle is advanced slowly until it has entered the epicardiumand fluid is obtained. The ECG can help determine when theneedle has contacted the epicardium. The cable of a precordiallead is attached to the aspirating needle with alligator clamps; con-tact with the epicardium is seen by ST segment elevation on theECG. During the procedure, drainage fluid must be checked forclotting. Although not entirely accurate, the guideline is that peri-cardial blood does not clot readily, whereas blood obtained frominadvertent puncture of one of the heart chambers does clot.

A resulting fall in central venous pressure and an associatedrise in blood pressure after withdrawal of pericardial fluid indi-cate that the cardiac tamponade has been relieved. The patientalmost always feels immediate relief. If there is a substantialamount of pericardial fluid, a small catheter may be left in placeto drain recurrent accumulation of blood or fluid. Pericardialfluid is sent to the laboratory for examination for tumor cells,bacterial culture, chemical and serologic analysis, and differentialblood cell count.

Complications of pericardiocentesis include ventricular orcoronary artery puncture, dysrhythmias, pleural laceration, gas-tric puncture, and myocardial trauma. After pericardiocentesis,the patient’s heart rhythm, blood pressure, venous pressure, andheart sounds are monitored to detect any possible recurrence ofcardiac tamponade. If it recurs, repeated aspiration is necessary.Cardiac tamponade may require treatment by open pericardialdrainage (pericardiotomy). The patient is ideally in an intensivecare unit.

PERICARDIOTOMYRecurrent pericardial effusions, usually associated with neoplasticdiseases, may be treated by a pericardiotomy (pericardial window).The patient receives a general anesthetic, but cardiopulmonarybypass is seldom necessary. A portion of the pericardium is ex-cised to permit the pericardial fluid to drain into the lymphaticsystem. Uncommonly, catheters are placed between the peri-cardium and abdominal cavity to drain the pericardial fluid.The nursing care is the same as that described for other cardiacsurgery (see Chap. 28).

MYOCARDIAL RUPTUREMyocardial rupture is a rare event. However, it can occur when amyocardial infarction, infectious process, cardiac trauma, pericar-dial disease, or other myocardial dysfunction weakens the cardiacmuscle (eg, ventricular aneurysm) substantially. Persistent elevationof the ST segment is an indication of ventricular aneurysm. In

many cases, the result of myocardial rupture is immediate death,even if the patient undergoes immediate cardiac surgery.

CARDIAC ARRESTCardiac arrest occurs when the heart ceases to produce an effec-tive pulse and blood circulation. It may be caused by a cardiacelectrical event, as when the HR is too fast (especially ventriculartachycardia or ventricular fibrillation) or too slow (bradycardia orAV block) or when there is no heart rate at all (asystole). Cardiacarrest may follow respiratory arrest; it may also occur when elec-trical activity is present but there is ineffective cardiac contractionor circulating volume, which is called pulseless electrical activ-ity (PEA). Formerly called electrical-mechanical dissociation(EMD), PEA can be caused by hypovolemia (eg, with excessivebleeding), cardiac tamponade, hypothermia, massive pulmonaryembolism, medication overdoses (eg, tricyclic agents, digitalis,beta-blockers, calcium channel blockers), significant acidosis, andmassive acute myocardial infarction.

Clinical ManifestationsConsciousness, pulse, and blood pressure are lost immediately.Ineffective respiratory gasping may occur. The pupils of the eyesbegin dilating within 45 seconds. Seizures may or may not occur.

The risk of irreversible brain damage and death increases withevery minute from the time that circulation ceases. The intervalvaries with the age and underlying condition of the patient. Dur-ing this period, the diagnosis of cardiac arrest must be made, andmeasures must be taken immediately to restore circulation.

Emergency Management: Cardiopulmonary ResuscitationThe ABCDs of basic cardiopulmonary resuscitation (CPR) areairway, breathing, circulation, and defibrillation (Guidelines2000 for Cardiopulmonary Resuscitation and Emergency Car-diovascular Care, 2000). Once loss of consciousness has beenestablished, the resuscitation priority for the adult in most casesis placing a phone call to activate the code team or the emer-gency medical system (EMS). Exceptions to this include neardrowning, drug or medication overdose, and respiratory arrestsituations, for which 1 minute of CPR should be performed be-fore activating the EMS. Because the underlying cause of arrestin an infant or child is usually respiratory, the priority is tobegin CPR and then activate the EMS after 1 minute of CPR.Because the care of the pediatric patient is individualized, thefollowing discussion on the care of a cardiac arrest patient ap-plies only to adults.

Resuscitation consists of the following steps:

1. Airway: maintaining an open airway2. Breathing: providing artificial ventilation by rescue breathing3. Circulation: promoting artificial circulation by external

cardiac compression4. Defibrillation: restoring the heartbeat (see Chap. 27)

NURSING ALERT The most reliable sign of cardiac arrest is theabsence of a pulse. In the adult and the child, the carotid pulse isassessed. In an infant, the brachial pulse is assessed. Valuable timeshould not be wasted taking the blood pressure, listening for theheartbeat, or checking proper contact of electrodes.

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If the patient is monitored or is immediately placed on themonitor using the multifunction pads or the quick-look paddles(found on most defibrillators) and the ECG shows ventriculartachycardia or ventricular fibrillation, defibrillation rather thanCPR is the treatment of choice. In this scenario, CPR is per-formed initially only if the defibrillator is not immediately avail-able. The survival rate decreases by 10% for every minute thatdefibrillation is delayed (Guidelines, 2000). If the patient has notbeen defibrillated within 10 minutes, the chance of survival isclose to zero. More information on defibrillation can be found inChapter 27.

MAINTAINING AIRWAY AND BREATHINGThe first step in CPR is to obtain an open airway. Any obviousmaterial in the mouth or throat should be removed. The chin isdirected up and back, or the jaw (mandible) is lifted forward. Therescuer “looks, listens, and feels” for air movement. An oropha-ryngeal airway is inserted if available. Two rescue ventilationsover 3 to 4 seconds are provided using a bag-mask or mouth-mask device (Fig. 30-5). An obstructed airway should be sus-pected when the rescuer cannot give the initial ventilations, andthe Heimlich maneuver or abdominal thrusts should be admin-istered to relieve the obstruction.

If the first rescue ventilations enter easily, the patient is venti-lated with 12 breaths per minute, and the open airway is main-tained. Endotracheal intubation is frequently performed by aphysician, nurse anesthetist, or respiratory therapist during a re-suscitation procedure (also called a code) to ensure an adequateairway and ventilation. The resuscitation bag device is then con-nected directly to the endotracheal tube.

Because of the risk of unrecognized esophageal intubation ordislodgement of the endotracheal tube (ET), tracheal intubationmust be confirmed by one technique from each of two differentmethods: a primary method (visualization of the ET through thevocal cords, auscultation of breath sounds in five areas on the chest,or bilateral chest expansion) and a secondary method (an esophagealdetector device [such as Ambu TubeChek] or an end-tidal CO2

detector). The end-tidal CO2 detectors available give qualitative(yes/no) or quantitative (measurable; ie, capnometry) results.Because delivery of CO2 is low in patients in cardiopulmonaryarrest, the qualitative devices are not as accurate in detectingincorrect placement as are esophageal detector devices (EDDs).There are two main types of EDD: a bulb type and a syringe type.

The bulb is collapsed or the plunger of the syringe compressedbefore its attachment to the ET; each creates a suction force at theend of the ET. If the ET is in the trachea, the presence of air inthe lungs and the rigid walls of the trachea allow re-inflation ofthe bulb or aspiration of the syringe. If the ET is in the esopha-gus, the suction pulls on the unsupported walls of the esophagus,causing them to collapse and preventing the bulb from re-inflating or the syringe to aspirate. A chest x-ray, which is fre-quently obtained after ET placement, is helpful in determiningwhether the ET is too high, too low, or in a main bronchus.However, a chest x-ray cannot confirm placement of an ET. TheET may be in the esophagus or the trachea and result in the sameappearance on the x-ray (Guidelines, 2000). Arterial blood gaslevels are measured to guide oxygen therapy.

RESTORING CIRCULATIONAfter performing ventilation, the carotid pulse is assessed and ex-ternal cardiac compressions are provided when no pulse is de-tected. If a defibrillator is not yet available but a process has beenput into place to obtain one, chest compressions are initiated.Compressions are performed with the patient on a firm surface,such as the floor, a cardiac board, or a meal tray. The rescuer (fac-ing the patient’s side) places the heel of one hand on the lowerhalf of the sternum, two fingerwidths (3.8 cm [1.5 inches]) fromthe tip of the xiphoid and positions the other hand on top of thefirst hand (Fig. 30-6) (Guidelines, 2000). The fingers should nottouch the chest wall.

Using the body weight while keeping the elbows straight, therescuer presses quickly downward from the shoulder area to de-liver a forceful compression to the victim’s lower sternum about3.8 to 5 cm (1.5 to 2 inches) toward the spine (Guidelines,2000). The chest compression rate is 80 to 100 times perminute. If only one rescuer is available, the rate is two ventila-tions to every 15 cardiac compressions. When two rescuers areavailable, the first person performs the cardiac compressions,pausing after the fifth compression, when the second rescuergives one ventilation over 1.5 to 2 seconds and at a tidal volumeof less than 1 L.

FIGURE 30-5 The chin lift and bag-and-mask technique for ventilatingpatients who need cardiopulmonary resuscitation.

FIGURE 30-6 Chest compressions in cardiopulmonary resuscitation(CPR) are performed by placing the heel of one hand on the lower half of thesternum and the other hand on top of the first hand. Elbows are kept straightand body weight is used to apply quick, forceful compressions to the lowersternum. For the most effective hand placement and outcome, the patient’schest should be bare.


When the code team or emergency medical personnel arrive,the patient is quickly assessed to determine cardiac rhythm and res-piratory status, as well as possible causes for the arrest. The specificsubsequent advanced life support interventions depend on the as-sessment results. For example, after the patient is placed on a car-diac monitor and ventricular fibrillation is detected, the patient willbe defibrillated up to three times, and then CPR will be resumed.However, if asystole is detected on the monitor, CPR is resumedimmediately while trying to identify the underlying cause, such ashypovolemia, hypothermia, or hypoxia. CPR may be stoppedwhen the patient responds and begins to breathe, the rescuers aretoo exhausted or at risk (eg, the building is at risk of collapsing) tocontinue CPR, or signs of death are obvious. If the patient does notrespond to therapies given during the arrest, the resuscitation effortmay be stopped or “called” by the physician. The decision to ter-minate resuscitation is based on medical considerations and takesinto account the underlying condition of the patient and thechances for survival.

FOLLOW-UP MONITORINGOnce successfully resuscitated, the patient is transferred to an in-tensive care unit for close monitoring. Continuous ECG moni-toring and frequent blood pressure assessments are essential untilhemodynamic stability is reestablished. Etiologic factors that pre-cipitated the arrest, such as metabolic or rhythm abnormalities,must be identified and treated. Possible contributing factors, suchas electrolyte or acid-base imbalances, need to be identified andcorrected. Selected medications, as described in Table 30-5, maybe used during and after resuscitation.

REFERENCES AND SELECTED READINGS

BooksAgency for Health Care Policy and Research. (1994). Heart failure:

Evaluation and care of patients with left-ventricular systolic dysfunction.Clinical Practice Guideline Number 11. AHCPR Publication

Table 30-5 • Medications Used in Cardiopulmonary Resuscitation

AGENT AND ACTION INDICATIONS NURSING CONSIDERATIONS

Oxygen—improves tissue oxygenationand corrects hypoxemia

Epinephrine (Adrenalin)—increases sys-temic vascular resistance and bloodpressure; improves coronary and cerebralperfusion and myocardial contractility

Atropine—blocks parasympathetic action;increases SA node automaticity and AVconduction

Sodium bicarbonate (NaHCO3)—correctsmetabolic acidosis

Magnesium—promotes adequate function-ing of the cellular sodium–potassiumpump

Vasopressin (Pitressin)—increases in-otropic action (contraction) of the heart

Administered to all patients with acute cardiacischemia or suspected hypoxemia, includingthose with COPD

Given to patients in cardiac arrest, especiallycaused by asystole or pulseless electrical activity; may be given if caused by ventric-ular tachycardia or ventricular fibrillation

Given to patients with symptomatic brady-cardia (hemodynamically unstable, frequentpremature ventricular contractions andsymptoms of ischemia)

Given to correct metabolic acidosis that is refractory to standard advanced cardiac lifesupport interventions (cardiopulmonary resuscitation, intubation, and respiratorymanagement)

Given to patients with torsades de pointes

An alternative to epinephrine when cardiac arrest is caused by ventricular tachycardia orventricular fibrillation

• Use 100% FiO2 during resuscitation.• Recognize that no lung damage occurs when

used for less than 24 hours.• Monitor dose by end-tidal CO2 or pulse

oximeter.

• Administer by IV push (IVP) or through theendotracheal (ET) tube.

• Avoid adding to IV lines that contain alka-line solution (eg, bicarbonate).

• Give rapidly as 2.0 to 2.5 mg IVP orthrough the ET tube.

• Be aware that less than 0.5 mg in the adultcan cause the heart rate to decrease to aworse bradycardia.

• Monitor patient for reflexive tachycardia.

• Administer initial dose of 1 mEq/kg IV; thenadminister the dose based on the base deficitcalculated from arterial blood gas values.

• Recognize that to prevent development ofrebound metabolic alkalosis, complete cor-rection of acidosis is not indicated

• May give diluted over 1–2 min or intra-venous push.

• Monitor for hypotension, asystole, brady-cardia, respiratory paralysis.

• Give 40 U IV one time only.

Critical Thinking Exercises

1. Your patient is a 55-year-old man who was diagnosedlast year with systolic HF (due to coronary artery disease)and was stabilized with lisinopril, Lasix, and metoprolol. Hefollows a low-sodium diet, with only an occasional indiscre-tion. He is complaining of a nagging cough. What are someof the possible causes for the cough? What would be key assessment factors that would help identify the cause? Whatmedical treatments and nursing interventions would be appropriate for each of the possible causes?

2. A 77-year-old female patient was readmitted for HF forthe third time in 2 months. Identify the factors that possiblycontribute to her readmission and that would need to be as-sessed. What interventions could be implemented to preventanother readmission? Describe the interaction (ie, behaviors,words, and communication techniques) that would demon-strate the concept of partnering with the patient.

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RESOURCES AND WEBSITES

The American College of Cardiology Heart House, 9111 Old George-town Road, Bethesda, MD 20814-1699; 1-800-253-4636, ext. 694or 301-897-5400; http://www.acc.org.

American Heart Association, 7320 Greenville Ave., Dallas, TX 75231;1-800-242-8721; http://www.americanheart.org.

Heart Failure Society of America, Court International, Suite 238-N, 2550University Avenue West, Saint Paul, MN 55144; 651-642-1633;http://www.abouthf.org.

Heartmates, Inc., PO Box 16202, Minneapolis, MN 55416; 952-929-3331; http://www.heartmates.com.

National Heart, Lung, and Blood Institute, National Institutes of Health,Building 31, Room 5A52, Bethesda, MD 20892; 301-592-8573;http://www.nhlbi.nih.gov.

National Institute on Aging, Building 31, Room 5C27, 31 Center Drive,MSC 2292, Bethesda, MD 20892; 301-496-1752; http://www.nih.gov/nia.

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