management of heart failure and treatment algorithm

ABSTRACTThe prevalence of heart failure is increasing among patients seen

in primary care settings. Proper diagnosis is essential, given that many treatmentconditions may mimic symptoms of heart failure. Early diagnosis and treatment

not only can increase a patient’s overall quality of life, but they can also signifi-cantly reduce rates of mortality and morbidity. Many pharmacologic options are

available to treat heart failure. Use of each medication in heart failure manage-ment needs to be carefully considered in selected patients. Close monitoring of

efficacy and side effects of each medication is vital.Keywords: Diagnosis, heart failure, pathophysiology, pharmacologic treatment,

treatment algorithm

Management of

Heart Failure and

Treatment Algorithm

Vicky Chang

530 The Journal for Nurse Practitioners - JNP September 2007

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www.npjournal.org The Journal for Nurse Practitioners - JNP 531

As the age of the general population increases, theprevalence and incidence of heart failure (HF)are also on the rise.1-3 HF is often a progressive

condition associated with significant rates of mortalityand morbidity that affects mainly the elderly. Five-yearmortality rates range from 35% in mild-to-moderate HFto up to 50% in advanced HF.The financial burden ofdirect HF care in 2006 was estimated at $29.6 billion inthe United States.1

Management of HF should include early identifica-tion of persons at risk of developing HF (Table 1) as wellas measures to improve quality of life among persons withthe disease.4,5 This article focuses on the management ofchronic HF in ambulatory care settings because most HFcare is being provided by primary care clinicians.

PATHOPHYSIOLOGYLeft ventricular (LV) dysfunction usually occurs as aresult of myocardial infarction, chronic hypertension, car-diomyopathy, or valvular heart disease.4-7 To maintain ade-quate tissue perfusion in the presence of LV dysfunction,several physiologic compensatory mechanisms are acti-vated.The two main compensatory mechanisms involvethe sympathetic nervous system (SNS) and the rennin-angiotensin-aldosterone system (RAAS). In an acute set-ting, these mechanisms are important to maintain home-ostasis. However, in chronic HF, these neurohormonescan cause damaging effects that lead to worsening of theHF symptoms.8,9

The activation of the SNS causes arterial vaso-constriction, which leads to increased blood pressure, heartrate, and cardiac afterload.As a result, cardiac workload andoxygen demand are increased, causing further cardiacischemia. In addition, increased renal vascular resistance by

activation of the SNS also reduces renal perfusion andincreases renin secretion. Furthermore, the release of reninleads to increased angiotensin II and aldosterone and, sub-sequently, activates the RAAS.The RAAS increases overallsodium retention and edema. It also reduces the effects ofbrain natriuretic peptide (BNP). BNP has vasodilatory anddiuretic properties and is secreted by ventricles when thetension of the ventricular walls is increased. In acute HF,BNP is initially secreted to maintain sodium balance andto increase vasorelaxation.Therefore, activation of theRAAS blunts the compensatory mechanisms of BNP inthe early stage of HF. In addition, aldosterone, which isincreased by the RAAS, can cause further reabsorption ofsodium.Aldosterone also was reported to increase tissuefibrosis, cause vascular remodeling, reduce heart rate vari-ability, and have predysrhythmic properties, all of whichcan lead of progression of HF.8,9

CLINICAL PRESENTATIONDepending on the severity of the disease and its cause,HF may present with various combinations of the fol-lowing symptoms4,9:

• Shortness of breath• Dyspnea on exertion• Paroxysmal nocturnal dyspnea• Weight gain as a result of fluid retention• Leg swelling• Cough• Fatigue; reduced exercise tolerance• Angina• Jugular venous distention• Hepatomegaly/ascites• Displaced apical impulse• Presence of S3 gallop

Table 1. Factors that Increase Risk of Developing Heart Failure4

Common Causes Less Common Causes • Ischemic heart disease • Familial hypertrophic cardiomyopathy • Diabetes • Postpartum cardiomyopathy • Hypertension • Thyroid hormone abnormality • Valvular heart disease • Connective tissue disorders • Increased alcohol intake • Toxin exposure (lead, arsenic, cobalt) • Overweight • Myocarditis • Cigarette smoking • Sarcoidosis • Hyperlipidemia • Hemochromatosis • Physical inactivity • Medication exposure (chemotherapy) • Sleep apnea


September 2007532 The Journal for Nurse Practitioners - JNP

The New York Heart Association (NYHA) classifica-tion is widely used to classify severity of the disease byassessing patients’ HF functional status (Table 2).

Many conditions may mimic HF symptoms; there-fore, it is important first to rule out other possible causesof the symptoms. Differential diagnoses for HF includecoronary ischemia, anemia, physical deconditioning,obesity, hepatic failure, renal failure, hypoalbuminemia,venous stasis, anxiety, and hyperventilation.4 The Fram-ingham Heart Study criteria were reported to be 100%sensitive and 78% specific for identifying persons withdefinite congestive HF (Table 3).10

INITIAL DIAGNOSTIC EVALUATIONPlasma BNPB-type natriuretic peptide is a cardiac neurohormonesecreted by the ventricles and is a significant predictor ofHF.The likelihood of a diagnosis of HF is small when BNPis less than 100 pg/mL.4,11 Therefore, it would be helpful toestablish a BNP baseline for patients with chronic HF.

EchocardiographyEchocardiography is the most useful noninvasive tool todiagnose HF. It reliably provides information on meas-

urements of cardiac chambers, wall thickness, LV func-tion, valvular function, and estimates of hemodynamicpressures.12,13

Most patients with HF have systolic HF.6 In systolicHF, patients usually have global hypokinesis causing areduction of LV ejection fraction (LVEF) to less than40%.Additional findings include elevated ventricular fill-ing pressure and increased pulmonary pressure.

Patients with diastolic HF usually have normal ornear normal LVEF. Left atrial enlargement in the absenceof mitral valve disease is highly indicative of LV diastolicdysfunction. In addition, abnormal blood flow across themitral valve can be detected when impaired LV relax-ation is present.14

Chest X-rayChest X-ray can be used as a screening tool to rule outpneumonia as a source of a patient’s symptoms. It alsoallows an assessment of heart size, although it is a poorindicator for ventricular function or dilatation. Presenceof cardiomegaly supports the diagnosis of HF, especiallywhen upper lobe pulmonary venous congestion is pres-ent.13 However, chest X-ray is not recommended for rou-tine HF follow-up.

Table 2. NYHA Functional Classification4

Functional Class Level of Physical ActivityClass I Ordinary physical activity does not cause symptoms.

Class II Slight limitation of physical activity. Comfortable at rest but ordinary activity causes symptoms.

Class III Marked limitation of physical activity. Comfortable at rest but less than ordinary activity causes symptoms.

Class IV Unable to carry on any physical activity without symptoms. Symptomatic even at rest.

Table 3. Framingham Heart Failure Criteria10

Major criteria Minor criteria • Paroxysmal nocturnal dyspnea • Bilateral ankle edema

• S3 gallop • Nocturnal cough

• Rales • Dyspnea on ordinary exertion

• Radiographic cardiomegaly • Hepatomegaly

• Acute pulmonary edema • Pleural effusion

• Increased central venous pressure • Decrease in vital capacity by one third from • (�16 cm H2O at right atrium) • maximum recorded

• Weight loss �4.5 kg in 5 days in response to treatment • Tachycardia (heart rate � 120 beats/min.)

• Hepatojugular reflux

Diagnosis of CHF requires the simultaneous presence of at least 2 major criteria or 1 major criterion in conjunction with 2 minor criteria.



ElectrocardiogramElectrocardiogram (EKG) is an important part of HFevaluation, although there are no specific EKG findingsthat are diagnostic for HF. Presence of a Q wave wouldsuggest a history of myocardial infarction and ischemicheart disease. In addition, heart rate and rhythm can pro-vide overall assessment of cardiac function. Most impor-tantly, LV hypertrophy is a common finding amongpatients with HF.4,12 Furthermore, prolongation of the

QRS duration is considered as an indication of poorprognosis in patients with HF.3

BiochemistryIn addition to BNP, it is essential to perform other labo-ratory tests to identify possible correctable triggering fac-tors for a patient’s HF exacerbation.These laboratory testsinclude complete blood count to rule out anemia andinfection; thyroid function test to rule out thyrotoxicosis;serum creatinine to assess renal function; electrolytes toassess potassium, sodium, and glucose status; and liverfunction test to rule out hepatic congestion as a result ofHF.4,6,12

ADDITIONAL DIAGNOSTIC TESTSThe following secondary diagnostic tests may be consid-ered for some, but not all, patients to help identify HFmanagement options.4-6,12

• exercise tolerance test• cardiac catheterization• holter monitor• pulmonary function test• nuclear cardiography• sleep study• 6-minute walk test

PHARMACOLOGIC TREATMENTBecause of the complexity of the disease, most patients withHF are routinely treated with polypharmacy. Most experts

recommend that medications be adjusted to dosages used inresearch protocols that have shown clinical benefits. Closemonitoring of these medications is essential to avoid com-plications and to maximize their clinical effects.

DiureticsSymptoms of HF usually result from fluid and sodiumretention. Diuretics can effectively reduce the symptoms ofpulmonary and systemic congestion and restore euvolemia.

However, diuretics were not shown toimprove mortality and should not beused alone in management of chronicHF.5,7 In addition, many patients mayexhibit HF symptoms without any signsof overt fluid overload; diuretics shouldnot be used as the first-line treatmentfor these patients and those remainasymptomatic.There are three main

categories of diuretics, and each works at a different sitein the renal tubule.

Thiazides. Thiazide diuretics block sodium transportin the distal convoluted tubule.When used alone, thi-azides are effective for treatment of hypertension but notof HF. In addition, the effects of thiazides are reducedwhen the glomerular filtration rate is below 30mL/min,6,7 and they would not be helpful to manypatients with HF who already have compromised kidneyfunction. However, metolazone (Zaroxolyn), a potent thi-azide, is effective when used along with a loop diuretic tosynergize the diuretic effect in patients with severe HF.9

When given in combination, metolazone usually is given30 minutes before the loop diuretic.

Loop diuretics.The loop diuretics are the diureticof choice for treatment of HF.The site of action for loopdiuretics is in the ascending limb of the loop of Henle.Patients with chronic HF may develop loop diureticresistance that will require either increasing the dosage ofthe loop diuretic or adding metolazone to the regimen.

Potassium-sparing diuretics. These diureticsinhibit sodium reabsorption in the collecting duct of thenephron and have mild direct diuretic and antihyperten-sive effects.They are often used as an adjunct agent tomaintain normokalemia.9 However, spironolactone(Aldactone) is also used as a neurohormonal antagonistfor patients with advanced HF.The use of spironolactoneis discussed in a later section. Renal insufficiency andhyperkalemia are contraindications for its use.

Because of the complexity of the disease,most patients with HF are routinely treated

with polypharmacy.



Clinical Use of DiureticsPatients should have baseline blood pressure,weight, serumglucose, and serum electrolytes done before starting adiuretic.4 Hydrochlorothiazide may be effective for patientswith hypertension and minimal fluid retention; otherwise,use a loop diuretic for all patients with HF.Both blood pres-sure and electrolytes should be repeated in 1 to 2 weeks.Some patients may be taught to increase the loop diureticdosage for 1 to 2 days if there is a weight gain of 2 poundsin 1 day or with increased HF symptoms.Persons takinghigher dosages of loop diuretics are at risk of developingprerenal syndrome if they are overdiuresed, causing elevationin blood urea nitrogen, creatinine, and potassium. If overdi-uresis occurs, the diuretics need to be withheld or reduced,and electrolytes and renal functions should be repeated in1 to 2 days before resuming treatment.To prevent diureticresistance, patents should always be maintained on the lowesteffective loop diuretic dosage and to reduce dietary sodiumintake.5 When a patient becomes resistant to one loopdiuretic, switching to a different loop diuretic may overcomethe resistance. If such strategy does not work, adding metola-zone 1 to 2 times a day 30 minutes before a loop diuretic isusually effective.4 A potassium-sparing diuretic can also beconsidered along with a loop diuretic, especially in the pres-ence of hypokalemia.

�-BlockersAfter a myocardial infarction, �-blockers may reduce mor-tality, LV remodeling, and hospital readmission.5,7 They sup-press both SNS and RAAS to provide cardiac protection.However, only three �-blockers,bisoprolol (Zebeta), carvedilol(Coreg), and sustained-releasemetoprolol XL (Toprol XL), havebeen approved for the manage-ment of HF.9 �-Blockers should beused with caution in patients withdiabetes, asthma, peripheral vasculardisease, hypotension, and brady-cardia.The combination of a�-blocker and an angiotensin-converting enzyme (ACE)inhibitor is recommended for management of patientswith chronic HF with LVEF of 40% or less.

Clinical Use of �-BlockersUnless contraindicated, patients should be placed on a �-blocker before discharge from the hospital after an MI or

stable HF. Patients should be started on a low dose andthe dose gradually increased every 2 weeks to reach targetdoses in 8 to 12 weeks.5 If worsening of HF symptomsoccurs during increasing dosing of a �-blocker, adjust-ments of diuretic and other medications may be triedbefore lowering the dosage of the �-blocker. Patientsmust avoid abrupt discontinuation of �-blockers becausethis may cause rebound hypertensive effects.

ACE Inhibitors and Angiotensin Receptor BlockersACE inhibitors and angiotensin receptor blockers(ARBs) reduce the effects of angiotensin II and subse-quently decrease aldosterone production. In studies,ACEinhibitors decreased rates of mortality, reduced hospitaladmissions, and increased functional status in patientswith NYHA classes II to IV.They also were shown tobenefit patients with asymptomatic systolic dysfunction.4,7

Common side effects of ACE inhibitors are cough,hyperkalemia, and, rarely, angioedema.4,5,9 They are usedwith caution when patients are also on a potassium-sparing diuretic. In general,ACE inhibitors are preferredto ARBs because ACE inhibitors were widely found tobe efficacious in clinical trials. However,ARBs usuallydo not cause cough and may be equally effective inmanagement of HF for patients who developed coughfrom ACE inhibitors.The benefits of ARBs were shownin the CHARM and Val-Heft trials that found signifi-cant reduction of cardiovascular mortality in patientswith NYHA class II to III HF with the use of candesar-tan and valsartan.15,16 However, the ELITE II trial

revealed nonsignificant increaseof sudden death or resuscitatedcardiac arrests in patients tak-ing losartan (Cozaar) comparedwith captopril.17 Therefore, val-sartan (Diovan) and candesar-tan (Atacand) are the preferredARBs used in the managementof HF.5 In addition, combina-tion of an ACE inhibitor and

candesartan were shown to reduce overall cardiovascularevent in patients with chronic HF in the CHARM-added trial.15 However, the combination of ACEinhibitor,ARB, and aldactone antagonist should not beused because of increased risks of hyperkalemia.5

ACE inhibitors are contraindicated in patients whoare pregnant, have a history of angioedema with previous

Common side effects ofACE inhibitors are

cough, hyperkalemia,and, rarely, angioedema.

530-536_YJNP459_Chang_CP 8/23/07 4:10 PM 34


exposure to an ACE inhibitor, or have severe hypoten-sion. Furthermore, caution is required in patients withelevated creatinine (�3 mg/dL), elevated serum potas-sium (�5.5 mmol/L), or bilateral renal artery stenosis.6

Clinical Use of ACE inhibitor and ARBs An ACE inhibitor may be used as a monotherapy forpatients with mild HF without fluid retention. Start patientson a low dose after obtaining baseline potassium and renalfunction. Potassium and creatinine must be repeated in 1 to2 weeks. Stop the medication immediately if there is a sig-nificant elevation in potassium or serum creatinine. If thereare no contraindications, the dosage can be slowly increasedto the target dosage used in clinical trials.9 Switch to Ata-cand or Diovan if cough persists on an ACE inhibitor.5

Aldosterone AntagonistsSpironolactone and Eplerenone suppress the neurohor-monal effects that cause the cascade of HF symptoms.Spironolactone was found to significantly reduce rates ofmortality, decrease hospitalization, and improve HF symp-toms among patients with NYHA class IV HF on stan-dard HF therapy.18 Renal insufficiency and hyperkalemiaare contraindications for their use. Close monitoring ofrenal function and serum potassium is required, especiallywhen a patient is also on an ACE inhibitor or ARB.Analdosterone antagonist is considered only if patientsremain symptomatic after treatment with diuretic,ACEinhibitor or ARB, and �-blocker.

Clinical Use of Aldosterone AntagonistsBaseline serum potassium and creatinine should beobtained and repeated in 3 days and periodically duringtreatment.4 The medication should be discontinued if anysignificant elevation of potassium or creatinine is noted.

Combination of Nitrates and HydralazineCombination of nitrates and hydralazine was found tobe more effective than placebo but less effective thanan ACE inhibitor in HF management. However, in asubsequent African-American Heart Failure Trial(A-HeFT), the combination of nitrate and hydralazineshowed significant benefits in African American patientswith NYHA class III to IV HF who were already onstandard drug treatment with diuretic,ACE inhibitoror ARB and �-blocker.4 Headache is a common

complaint, and lower dosage should be started withgradual increase in dosage.

Clinical use of Combined Nitrate and HydralazineGiven the beneficial finding of the A-HeFT, combinednitrate and hydralazine should be considered in AfricanAmerican patients with NYHA class III and IV HF who arealready on the standard ACE inhibitor or ARB, �-blocker,and aldactone.4 This is also a possible alternative treatmentfor patients who are unable to tolerate ACE inhibitors.6,7 Toprevent nitrate-related headaches, start on a low dose andhave the patient take Tylenol 30 minutes before takingnitrate.BiDil is a drug that combines hydralazine 37.5 mgand isosorbide dinitrate 20 mg in one pill. However, separatenitrate and hydralazine can be used if cost is a concern.Patient compliance needs to be monitored because this regi-men requires dosing 3 to 4 times a day.

DigitalisUse of digoxin in treatment of HF is controversial, espe-cially in patients with low LVEF, normal sinus rhythm, orwithout history of HF symptoms.5 Several studies showedshort-term treatment with digoxin improved HF symp-toms, quality of life, and exercise tolerance.5,7 The DigitalisInvestigation Group Trial showed that in patients withLVEF of 45% or less and already on diuretic and ACEinhibitor, when compared with a placebo, patients in thedigoxin group were less likely to develop worsening HFand to be hospitalized. However, there was no differencein mortality rate.4 Digoxin provides positive inotropiceffects and reduces plasma noradrenaline and sympatheticnerve activity.Therefore, digoxin is most beneficial forpatients with HF who also have atrial fibrillation. Other-wise, digoxin should be considered only as an add-ontherapy for patients remaining symptomatic despite ACEinhibitor, �-blocker, diuretic, and aldosterone antagonist.5

Contraindications to the use of digoxin include second-and third-degree atrioventricular block, sick sinus syn-drome, and severe bradycardia.

Clinical Use of DigitalisDigoxin should not be used as a primary HF therapy. Noloading dose is needed for patients with chronic HF.6

Baseline EKG, renal function, and electrolytes will needto be obtained. Digoxin levels need to be monitored andkept below 1.0 ng/mL.4,5 In addition, serum potassium,



magnesium, and renal function should be checked peri-odically to avoid digoxin toxicity.4-6

OTHER TREATMENTCardiac resynchronization therapy, such as cardioverter-defibrillators and pacemakers, are increasingly implanted inpatients with advanced HF.Outpatient infusion therapy withLasix also is becoming popular for treatment of refractoryHF.However, these treatments are usually managed by cardi-ology specialists and are beyond the scope of this article.Patients who continue to exhibit HF symptoms despite

maximal pharmacologic treatment should be referred tospecialists for further interventions.

CLINICAL PATHWAYTreatments of diastolic HF are not fully established.Tighter control of both systolic and diastolic bloodpressures remains the goal in treating asymptomaticdiastolic HF.5 However, management of systolic HF iswell defined.A step-by-step treatment algorithm forsystolic HF management was developed to guidetherapeutic approach (Figure 1).

LVEF � 40%

ACE inhibitor ARB

Increase to target dose Tolerant toARB

Continue toMonitor symptoms

Symptoms controlled

Signs of fluid overload

Loop diuretic Beta blocker

Symptom controlled.Maintain on lowestEffective dosage

Increase loop diuretic dosageAnd introduce beta blocker

Able to tolerate it

Titrate up totarget dosage

Increase ACE inhibitorand continue to titrate betablocker and loop diuretic to

target dose

Add metolazone

Symptom improvement

AfricanAmericanpatients

Continue to monitor symptomsand titrate medications as

needed.Symptom improvement

Combined nitrate andhydralazine

Consider digoxin(earlier if atrial

Fibrillation.)

Unable to tolerate

Normal K and Cr

Yes

Yes

Yes

Yes

Yes

Yes

Yes

No

No

No

No improvement

No

No improvement

No

No

No improvement

OR (if unableto toleratebeta blocker)

Add Aldactone(monitor K and CY)

No

Figure 1. HF treatment algorithm for patients without MI.



SUMMARYHF therapies are complex, and they require significantoversight from primary care clinicians. It takes a carefulbalance to slowly titrate the medications to control thesymptoms without causing potentially harmful sideeffects. Many patients with HF can lead productive livesfor many years with proper management of theirmedical treatment.

References:

1. Centers for Disease Control and Prevention. Heart Failure Fact Sheet. 2006.2. Hauptman PJ, Havranek EP. Integrating palliative care into heart failure care.

Arch Inter Med. 2005;165(4):374-378. http://www.cdc.gov/DHDSP/library/fs_heart_failure.html

3. Rivera DA, Bristow MR: Cardiac resynchronization—a heart failureperspective. Ann Noninv Electrocard. 2005;10(4):S16-23.

4. Heart Failure Society of America. HSFA 2006 comprehensive heart failurepractice guideline. J Card Fail. 2006;12(1):e1-e122.

5. ACC/AHA 2005 guideline update for the diagnosis and management ofchronic heart failure in the adult. Washington, DC: American College ofCardiology Foundation and the American Heart Association, 2005. p. 1-82.

6. Remme WJ, Swedberg K; Task Force on Heart Failure of the EuropeanSociety of Cardiology. Guidelines for the diagnosis and treatment of chronicheart failure. Eur Heart J. 2001;22(17):1527-1560.

7. Prendergast HM, Bunney EB. Management of chronic heart failure: an olddisease with a new face. Emerg Med Australas. 2005;17(2):143-151.

8. Odedra K, Ferro A. Neurohormones and heart failure: the importance ofaldosterone. Int J Clin Pract. 2006;60(7):835-846.

9. Greenberg BH, Hermann DD. Contemporary diagnosis and management ofheart failure. Newtown, PA.: Handbooks in Health Care, 2002. p. 5-269.

10. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history ofcongestive heart failure: the Framingham study. N Engl J Med.1971;285(26):1441-1446.

11. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement ofB-type natriuretic peptide in the emergency diagnosis of heart failure.N Engl J Med. 2002;347(14):161-167.

12. Cleland JG, Habib F. Assessment and diagnosis of heart failure.J Intern Med. 1996;23(4):317-325.

13. Sharpe N. Management principles: much more to be gained. In: Sharpe N,editor. Heart failure management. London, United Kingdom: Matinez Dunitz,2000. p. 15-27.

14. Chatterjee K. Diastolic and systolic heart failure—similarities anddifferences, part 1. Cardiol Rounds. 2005;9(9):1-6.

15. Pfeiffer MA, Swedberg K, Granger CB, et al. Effects of candesartan onmortality and morbidity in patients with chronic heart failure: theCHARM-Overall programme. Lancet. 2003;362(9386):759-766.

16. Cohn J, Tognoni G; Valsartan Heart Failure Trial Investigators. A randomizedtrial of angiotensin receptor blocker valsartan in chronic heart failure.N Engl J Med. 2001;345(23):1667-1675.

17. Pitt B, Poole-Wilson PA, Segal R, et al. Effect of losartan compared withcaptopril on mortality in patients with symptomatic heart failure:randomized trial—the Losartan Heart Failure Survival Study, ELITE II.Lancet. 2000;355(9215):1582-1587.

18. Pitt B, Zannad F, Remme W, et al. The effect of spironolactone on morbidityand mortality in patients with severe heart failure. N Engl J Med.1999;341(10):709-717.

Vicky Chang, MSN,APRN, BC-ADM, is affiliated with theDepartment of Veterans Affairs,VA Connecticut HealthcareSystem,West Haven Campus. She can be reached [email protected]. In conjunction with national ethicalstandards, this author reports no relationship with business orindustry that represents a conflict of interest.

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