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The Vicious Cycle of The Vicious Cycle of Heart FailureHeart Failure
Natalie Bermudez, RN, BSN, MSNatalie Bermudez, RN, BSN, MS
Telemetry Telemetry CourseCourse
Clinical Educator for TelemetryClinical Educator for Telemetry
Heart FailureHeart FailureCongestive heart failure is the only Congestive heart failure is the only
cardiovascular disorder with increasing cardiovascular disorder with increasing incidence and mortality.incidence and mortality.
Hospital admissions are rapidly increasing, and Hospital admissions are rapidly increasing, and has a major impact on quality of life and has a major impact on quality of life and
financial resources.financial resources.
In fact, advanced heart failure has become the In fact, advanced heart failure has become the most costly medical syndrome.most costly medical syndrome.
(Vavouranakis et al, 2003, p. 105)(Vavouranakis et al, 2003, p. 105)
StatisticsStatisticsAccording to Chojnowski (2008), According to Chojnowski (2008),
“hospital discharges for the diagnosis “hospital discharges for the diagnosis of heart failure increased a whopping of heart failure increased a whopping 175% between 1979 and 2004, with 175% between 1979 and 2004, with
30% to 60% of patients being 30% to 60% of patients being readmitted within 6 months” readmitted within 6 months” (p. 50).(p. 50).
““Heart failure accounts for nearly 1 Heart failure accounts for nearly 1 million hospitalizations each year” million hospitalizations each year”
(Moser & Riegel, 2008, p. 916).(Moser & Riegel, 2008, p. 916).
More StatisticsMore StatisticsAccording to the AHA:According to the AHA:
More than 5 million adults in the U.S. had a HF diagnosis in 2004More than 5 million adults in the U.S. had a HF diagnosis in 2004(Chojnowski, 2007, p. 50)(Chojnowski, 2007, p. 50)
While deaths overall decreased 2% between 1994 and 2004, deaths While deaths overall decreased 2% between 1994 and 2004, deaths from HF increased 28%from HF increased 28%
(Chojnowski, 2007, p. 50)(Chojnowski, 2007, p. 50)
According to the American Heart Association’s According to the American Heart Association’s publication, publication, Heart Disease and Stroke Statistics: 2008 Heart Disease and Stroke Statistics: 2008
Update At-A-Glance, Update At-A-Glance, the estimated indirect and direct the estimated indirect and direct cost of hospitalization for acute decompensated heart cost of hospitalization for acute decompensated heart
failure (ADHF) in the United States is $34.8 billion.failure (ADHF) in the United States is $34.8 billion. (expected cost for 2007 was $33.2 billion)(expected cost for 2007 was $33.2 billion)
More StatisticsMore Statistics
On a yearly basis, 12 to 15 million office visits On a yearly basis, 12 to 15 million office visits and 6.5 million hospital visits are due to HFand 6.5 million hospital visits are due to HF
(Wynne, Woo, & Olyaei, 2007)(Wynne, Woo, & Olyaei, 2007)
““Despite aggressive investigation into Despite aggressive investigation into treatment options, until very recently the treatment options, until very recently the
5-year mortality rate was 50%”5-year mortality rate was 50%”(Wynne, Woo, & Olyaei, 2007, p. 1009)(Wynne, Woo, & Olyaei, 2007, p. 1009)
ReadmissionsReadmissionsAs many as 50% of patients with As many as 50% of patients with
ADHF are readmitted within 6 ADHF are readmitted within 6 months of discharge” months of discharge” (Moser & Riegel, 2008).(Moser & Riegel, 2008).
Nonadherence to medications or dietNonadherence to medications or diet Failure to seek medical care when symptoms ariseFailure to seek medical care when symptoms arise Receiving inappropriate therapyReceiving inappropriate therapy Decreased length of stayDecreased length of stay
Premature discharge before all medical issues have been addressed; not Premature discharge before all medical issues have been addressed; not meeting D/C criteriameeting D/C criteria
Inadequate patient education (NB)Inadequate patient education (NB)
What Is HF?What Is HF?HF is the inability of the heart to HF is the inability of the heart to
maintain adequate cardiac output to maintain adequate cardiac output to meet metabolic demands of the bodymeet metabolic demands of the body
More commonly occurs in the left More commonly occurs in the left ventricleventricle
But also happens on the right, but is But also happens on the right, but is usually preceded by left-sided heart usually preceded by left-sided heart
failurefailure
HF’s Main IssueHF’s Main Issue
Leads to fluid overload and Leads to fluid overload and inadequate tissue inadequate tissue
perfusion!!!perfusion!!!
Heart FailureHeart FailureAcute versus Chronic HFAcute versus Chronic HF
Left-sided versus Right-sidedLeft-sided versus Right-sided
Systolic versus DiastolicSystolic versus Diastolic
Heart FailureHeart FailureHF can severely restrict a person’s HF can severely restrict a person’s
ability to perform ADL’sability to perform ADL’s
Affects person’s quality of lifeAffects person’s quality of life
Prognosis depends on underlying Prognosis depends on underlying cause and treatment cause and treatment
Heart FailureHeart FailurePATHOPHYSIOLOGY:PATHOPHYSIOLOGY:
Underlying cause determines whether Underlying cause determines whether HF is chronic or acuteHF is chronic or acute
Associated with systolic or diastolic Associated with systolic or diastolic overloading and myocardial weaknessoverloading and myocardial weakness
Heart FailureHeart FailurePATHOPHYSIOLOGY:PATHOPHYSIOLOGY:
As stress on the heart muscle reaches a As stress on the heart muscle reaches a critical level, the muscle’s contractility critical level, the muscle’s contractility
decreasesdecreases (Frank-Starling)(Frank-Starling) and CO and CO ↓↓
Venous input to the ventricles does not Venous input to the ventricles does not change!change!
Systolic Heart Systolic Heart FailureFailure
PathophysiologyPathophysiology
Results in decreased blood volume Results in decreased blood volume ejected from the ventricleejected from the ventricle
SNS stimulated & releases epinephrine SNS stimulated & releases epinephrine & norepinephrine & norepinephrine → ↑ HR to → ↑ HR to
maintain COmaintain CO
PathophysiologyPathophysiologyNegative Effects of SNS Stimulation:Negative Effects of SNS Stimulation:
Angiotensin-converting enzyme (vasodilator) Angiotensin-converting enzyme (vasodilator) is activated in pulmonary vessels is activated in pulmonary vessels → ↑ B/P → ↑ B/P
and afterloadand afterload
Angiotensin II Angiotensin II → aldosterone released → Na → aldosterone released → Na & Fluid Retention → Stimulates thirst & Fluid Retention → Stimulates thirst
centercenter
PathophysiologyPathophysiologyNegative Effects of SNS stimulation:Negative Effects of SNS stimulation:
What is the end result of this???What is the end result of this???
FLUID VOLUME OVERLOAD!!!FLUID VOLUME OVERLOAD!!!
Causes Causes ↑ workload of the heart!↑ workload of the heart!
PathophysiologyPathophysiologyCounterregulatory Effects:Counterregulatory Effects:
Release of natriuretic peptides, Release of natriuretic peptides, prostaglandins, and nitric oxideprostaglandins, and nitric oxide
Natriuretic Peptides:Natriuretic Peptides:
ANP (found mainly in the atria) ANP (found mainly in the atria)
BNP (found mainly in the ventricles)BNP (found mainly in the ventricles)
PathophysiologyPathophysiologyCounterregulatory Effects:Counterregulatory Effects:
Brain Natriuretic PeptideBrain Natriuretic Peptide
Secreted by the ventricles with ventricular Secreted by the ventricles with ventricular volume expansion and pressure overloadvolume expansion and pressure overload
PathophysiologyPathophysiologyEffects of BNP:Effects of BNP:
They are released from the overdistended They are released from the overdistended cardiac chamberscardiac chambers
They promote vasodilation and natriuresisThey promote vasodilation and natriuresis
When released they also inhibit renin When released they also inhibit renin and aldosterone releaseand aldosterone release
PathophysiologyPathophysiologyCounterregulatory Effects versus Counterregulatory Effects versus
Negative Effects of SNS Negative Effects of SNS stimulation:stimulation:
This effect is not strong enough to This effect is not strong enough to overcome the negative effects of the overcome the negative effects of the
other mechanismsother mechanisms
PathophysiologyPathophysiologyIn the End, there is still…In the End, there is still…
↑↑ Workload Workload → → ↓ myocardial contractility → ↓ myocardial contractility → Increased afterload ventricular dilation → Increased afterload ventricular dilation → Increasing workload → leads to ventricular Increasing workload → leads to ventricular
hypertrophyhypertrophy
Vicious Cycle of HFVicious Cycle of HF
The heart does not pump sufficient blood toThe heart does not pump sufficient blood to
body, which causes the body to stimulatebody, which causes the body to stimulate
the heart to work harder; the heart cannotthe heart to work harder; the heart cannot
respond (due to myocardial damage) and, in respond (due to myocardial damage) and, in spite of counterregulatory mechanisms,spite of counterregulatory mechanisms,
the failure becomes worse.the failure becomes worse.
Diastolic Heart FailureDiastolic Heart Failure
Develops because of continued increased Develops because of continued increased workload, which responds by increasing the workload, which responds by increasing the
number and size of myocardial cells (i.e., number and size of myocardial cells (i.e., ventricular hypertrophy and altered cell ventricular hypertrophy and altered cell
functioning). functioning).
This causes decreased ventricular filling This causes decreased ventricular filling
and decreased CO stimulating the SNS in and decreased CO stimulating the SNS in the same fashion as systolic HF. the same fashion as systolic HF.
Etiology Etiology Coronary Artery Coronary Artery
DiseaseDisease Myocardial Myocardial
InfarctionInfarction Hypertension Hypertension (S or P)(S or P)
Rheumatic HDRheumatic HD Connective Tissue Connective Tissue
DiseaseDisease
Congenital HDCongenital HD Thyroid Thyroid
AbnormalitiesAbnormalities CardiomyopathyCardiomyopathy Valvular DiseasesValvular Diseases Persistent Persistent
TachydysrhythmiasTachydysrhythmias Toxins (chemo)Toxins (chemo) ETOH AbuseETOH Abuse
Etiology Etiology The chief contributors to the development The chief contributors to the development
of HF are coronary artery disease and of HF are coronary artery disease and hypertension, both of which are found in hypertension, both of which are found in 40% of patients with HF” 40% of patients with HF” (Moser & Riegel, 2008, p. 916).(Moser & Riegel, 2008, p. 916).
Regardless of the cause of HF, it is a Regardless of the cause of HF, it is a chronic condition that becomes chronic condition that becomes progressively worse, culminating in the progressively worse, culminating in the patient’s premature death patient’s premature death (Moser & Riegel, 2008, p. 916).(Moser & Riegel, 2008, p. 916).
Signs & SymptomsSigns & Symptoms
Dyspnea on ExertionDyspnea on Exertion OrthopneaOrthopnea TachypneaTachypnea Paroxysmal Nocturnal Paroxysmal Nocturnal
DyspneaDyspnea Crackles (bases)Crackles (bases) Dullness (percussion)Dullness (percussion) Tactile FremitusTactile Fremitus
Displaced Apical Displaced Apical HeartbeatHeartbeat
TachycardiaTachycardia ConfusionConfusion Anxiety/RestlessnessAnxiety/Restlessness Impaired MemoryImpaired Memory DiaphoresisDiaphoresis Cool extremitiesCool extremities OliguriaOliguria
Left-Sided HFLeft-Sided HF
Signs & Signs & SymptomsSymptoms
FatigueFatigue AscitesAscites
Enlarged SpleenEnlarged Spleen Enlarged LiverEnlarged Liver
JVDJVD
AnorexiaAnorexia Edema Hands & Edema Hands &
FingerFinger Dependent EdemaDependent Edema
Increased peripheral Increased peripheral venous pressurevenous pressure
Right-Sided HFRight-Sided HF
Diagnostic EvaluationDiagnostic Evaluation ECHO ECHO → determines EF %→ determines EF %
Chest X-ray → fluid in pulmonary Chest X-ray → fluid in pulmonary space & possible underlying causespace & possible underlying cause
EKG → determine underlying causeEKG → determine underlying cause BUN/Creatinine → assess for renal BUN/Creatinine → assess for renal
failurefailure BNP → high levels indicate CHF (> BNP → high levels indicate CHF (>
100)100) Electrolytes & CBCElectrolytes & CBC
4 Stages of HF4 Stages of HFStage AStage A
Patients at risk for developing heart Patients at risk for developing heart failure are addressed almost failure are addressed almost exclusively in the ACC/AHA exclusively in the ACC/AHA
guidelinesguidelines
First-line treatment is lifestyle First-line treatment is lifestyle modifications and drug therapy with modifications and drug therapy with
ACE inhibitorsACE inhibitors
4 Stages of HF4 Stages of HFStage BStage B
Patients with left ventricular Patients with left ventricular dysfunction who have not developed dysfunction who have not developed
symptomssymptoms
Treatment includes lifestyle Treatment includes lifestyle modifications and drug therapy with modifications and drug therapy with ACE inhibitors, BB’s, and/or cardiac ACE inhibitors, BB’s, and/or cardiac
glycosides (for patients with a-fib only)glycosides (for patients with a-fib only)
4 Stages of HF4 Stages of HFStage CStage C
Patients with left ventricular Patients with left ventricular dysfunction with current symptoms dysfunction with current symptoms or prior symptoms of heart failureor prior symptoms of heart failure
Treatment includes lifestyle Treatment includes lifestyle modifications and drug therapy with modifications and drug therapy with
ACEIs or ARBs, BB’s, cardiac ACEIs or ARBs, BB’s, cardiac glycosides, and a diureticglycosides, and a diuretic
4 Stages of HF4 Stages of HFStage DStage D
Patients with refractory end-stage Patients with refractory end-stage heart failureheart failure
Treatment is usually prescribed by a Treatment is usually prescribed by a specialistspecialist
Acute HF ExacerbationAcute HF Exacerbation
Supplemental Oxygen Therapy & Supplemental Oxygen Therapy & Diuretics for Diuretics for
Acute Decompensated HFAcute Decompensated HF
SYMPTOMATIC TREATMENTSYMPTOMATIC TREATMENT
AnticoagulantsAnticoagulants
Used for patients with Used for patients with HF who also have HF who also have
chronic atrial chronic atrial fibrillationfibrillation
(Wynne, Woo, & Olyaei, 2007, p. 1012)(Wynne, Woo, & Olyaei, 2007, p. 1012)
Pharmacologic ManagementPharmacologic Management
PO/IV Medications:PO/IV Medications: ACE inhibitorsACE inhibitors (Vasotec) (Vasotec)
Angiotensin II Receptor BlockersAngiotensin II Receptor Blockers (ARBs) (Diovan) (ARBs) (Diovan) Vasodilators (nitroglycerin, nesiritide, nitroprusside)Vasodilators (nitroglycerin, nesiritide, nitroprusside)
Beta-blockers (Coreg, Lopressor, Toprol)Beta-blockers (Coreg, Lopressor, Toprol) DiureticsDiuretics (Lasix, Aldactone, HCTZ, Zaroxolyn) (Lasix, Aldactone, HCTZ, Zaroxolyn)
Digitalis (digoxin – Lanoxin)Digitalis (digoxin – Lanoxin) Calcium channel blockers (Norvasc, Plendil)Calcium channel blockers (Norvasc, Plendil)
Anticoagulants and AntiplateletsAnticoagulants and Antiplatelets Inotropics (dobutamine, dopamine, milrinone)Inotropics (dobutamine, dopamine, milrinone)
Aldosterone AntagonistsAldosterone Antagonists
ACEIs & ARBsACEIs & ARBs
Act on the R-A-A Act on the R-A-A system to decrease system to decrease
preload and afterloadpreload and afterload
(Wynne, Woo, & Olyaei, 2007, p. 1012)(Wynne, Woo, & Olyaei, 2007, p. 1012)
ACEIs & ARBsACEIs & ARBs
ACEIs are the drug of choice in the ACEIs are the drug of choice in the treatment of HF treatment of HF (prevents HF (prevents HF
exacerbation)exacerbation)
ACEIs affect both preload and afterload ACEIs affect both preload and afterload through vasodilatory effects, decrease the through vasodilatory effects, decrease the incidence of remodeling by reducing the incidence of remodeling by reducing the
local generation and action of angiotensin local generation and action of angiotensin II in the heart muscle, and prevent II in the heart muscle, and prevent neurohormonal counterregulatory neurohormonal counterregulatory
mechanisms that worsen heart failure mechanisms that worsen heart failure through their action on the R-A-A systemthrough their action on the R-A-A system
((Wynne, Woo, & Olyaei, 2007, p. 1014)Wynne, Woo, & Olyaei, 2007, p. 1014)
ACEIs & ARBsACEIs & ARBs
As monotherapy or in As monotherapy or in combination with other combination with other
drugs, ACEIs are drugs, ACEIs are superior to all other superior to all other
drugs and drug drugs and drug combinations used to combinations used to
treat HFtreat HF(Wynne, Woo, & Olyaei, 2007, p. 1014)(Wynne, Woo, & Olyaei, 2007, p. 1014)
ACEIs & ARBsACEIs & ARBs
Losartan (Cozaar) is Losartan (Cozaar) is officially the only ARB officially the only ARB approved for treatment approved for treatment
of HF.of HF.
(Wynne, Woo, & Olyaei, 2007, p. 1015)(Wynne, Woo, & Olyaei, 2007, p. 1015)
Beat-Adrenergic BlockersBeat-Adrenergic Blockers
Affect the SNS Affect the SNS counterregulatory counterregulatory mechanism of HFmechanism of HF
(Wynne, Woo, & Olyaei, 2007, p. 1012)(Wynne, Woo, & Olyaei, 2007, p. 1012)
Pharmacologic ManagementPharmacologic Management
WARNING:WARNING:Beta-Blocker therapy with Beta-Blocker therapy with diastolicdiastolic HF may HF may
cause exacerbation of symptomscause exacerbation of symptoms
Negative Inotropic & Chronotropic EffectsNegative Inotropic & Chronotropic Effects
Decreases heart rateDecreases heart rate
Decreases contractilityDecreases contractility
Vasodilators/NitratesVasodilators/Nitrates
Improve systolic and Improve systolic and diastolic ventricular diastolic ventricular
function by improving function by improving oxygen transport to the oxygen transport to the
myocardium for myocardium for patients with HF who patients with HF who
also have anginaalso have angina(Wynne, Woo, & Olyaei, 2007, p. 1012)(Wynne, Woo, & Olyaei, 2007, p. 1012)
AntiplateletsAntiplatelets
Used to prevent Used to prevent myocardial infarction myocardial infarction and death in patients and death in patients
with HF who have with HF who have underlying CADunderlying CAD
(Wynne, Woo, & Olyaei, 2007, p. 1012)(Wynne, Woo, & Olyaei, 2007, p. 1012)
Pharmacologic ManagementPharmacologic Management
IV InfusionsIV Infusions::
Natrecor drip (nesitiride) – elevated BNP levels; BP Natrecor drip (nesitiride) – elevated BNP levels; BP monitored closelymonitored closely
Primacor drip (milrinone) – promotes vasodilation; BP Primacor drip (milrinone) – promotes vasodilation; BP monitored closelymonitored closely
Dobutrex drip (dobutamine) – increases cardiac Dobutrex drip (dobutamine) – increases cardiac contractility (may cause tachydysrhythmias)contractility (may cause tachydysrhythmias)
Lanoxin (digoxin)Lanoxin (digoxin)
Positive Inotropic Effects:Positive Inotropic Effects:Improves cardiac contractilityImproves cardiac contractility
Negative Chronotropic Effects:Negative Chronotropic Effects:Decreases heart rateDecreases heart rate
Main uses are with CHF and supraventricular Main uses are with CHF and supraventricular tachycardiastachycardias
Cardiac GlycosideCardiac Glycoside
Lanoxin (digoxin)Lanoxin (digoxin)
May be administered PO or IVMay be administered PO or IV
Caution: If given IVP, need to administer Caution: If given IVP, need to administer slowly over 5 minutes (at least)slowly over 5 minutes (at least)
Inform monitor technician prior to Inform monitor technician prior to administrationadministration
Lanoxin (digoxin)Lanoxin (digoxin)ATTENTION!!!ATTENTION!!!
For severe digoxin toxicity, For severe digoxin toxicity, administer…administer…
Digibind (Digoxin Immune FAB)Digibind (Digoxin Immune FAB)
380 – 760 mg IV380 – 760 mg IV
Lanoxin (digoxin)Lanoxin (digoxin)
Take apical pulse for 1 full minute prior to Take apical pulse for 1 full minute prior to administrationadministration
If less than 60, hold and notify physicianIf less than 60, hold and notify physician
Monitor digoxin levels to evaluate potential Monitor digoxin levels to evaluate potential toxicitytoxicity
S/S – “Yellow Lights”S/S – “Yellow Lights”
Lasix Lasix (furosemide)(furosemide)
Inhibits reabsorption of Na & Cl @ Inhibits reabsorption of Na & Cl @ proximal and distal tubule and in the proximal and distal tubule and in the
loop of Henleloop of Henle
Main uses are with CHF, pulmonary Main uses are with CHF, pulmonary edema, and Hypertension edema, and Hypertension
Loop DiureticLoop Diuretic
Lasix (furosemide)Lasix (furosemide)
May be administered PO or IVMay be administered PO or IV
Caution: If given IVP, need to Caution: If given IVP, need to administer slowly 20 mg/minadminister slowly 20 mg/min
Lasix (furosemide)Lasix (furosemide)
Monitor B/P prior to and following Monitor B/P prior to and following administrationadministration
Monitor urine output, edema, and lung Monitor urine output, edema, and lung soundssounds
Monitor serum electrolytes (K, Na)Monitor serum electrolytes (K, Na)
Natrecor (nesiritide)Natrecor (nesiritide)
Human BNP bonds to the receptor on Human BNP bonds to the receptor on vascular smooth muscle and endothelial vascular smooth muscle and endothelial
cellscells
Newer medication – use has not become Newer medication – use has not become widespread yet…widespread yet…
Vasodilator – Human BNPVasodilator – Human BNP
Therapeutic Therapeutic InterventionsInterventions
Intraaortic Balloon Pump (IABP)Intraaortic Balloon Pump (IABP)
Most widely used mechanical support deviceMost widely used mechanical support device
Increases blood flow to heart muscle, decreases Increases blood flow to heart muscle, decreases the workload of the heart, and may be used in the workload of the heart, and may be used in
the presence cardiogenic shock and ADHF the presence cardiogenic shock and ADHF caused by MIcaused by MI
(Moser & Reigel, 2008, p. 925)(Moser & Reigel, 2008, p. 925)
Therapeutic Therapeutic InterventionsInterventions
Intraaortic Balloon Pump (IABP)Intraaortic Balloon Pump (IABP)
It is placed proximal to the aorta and inflates It is placed proximal to the aorta and inflates when the heart relaxeswhen the heart relaxes
This forces the blood forward to perfuse the This forces the blood forward to perfuse the periphery and backward to fill the coronary periphery and backward to fill the coronary
arteriesarteries
(Moser & Reigel, 2008, p. 925)(Moser & Reigel, 2008, p. 925)
Therapeutic Therapeutic InterventionsInterventions
Left Ventricular Assistive Device (LVAD)Left Ventricular Assistive Device (LVAD)
Used to control acute reversible HF resulting in Used to control acute reversible HF resulting in cardiogenic shock, which is often caused by AMIcardiogenic shock, which is often caused by AMI
Mechanical support may augment the patient’s Mechanical support may augment the patient’s circulation until myocardium improves enough for circulation until myocardium improves enough for
patient to undergo revascularizationpatient to undergo revascularization
(Moser & Reigel, 2008, p. 925)(Moser & Reigel, 2008, p. 925)
DIETARY MANAGEMENTDIETARY MANAGEMENT
RestrictionsRestrictionsLow sodium diet Low sodium diet
(2 – 3 grams/day)(2 – 3 grams/day)
Limited fluid intakeLimited fluid intake
Nursing Interventions & Nursing Interventions & ConsiderationsConsiderations
MonitoringMonitoringPhysical AssessmentPhysical Assessment
Inspection, Auscultation, PalpationInspection, Auscultation, Palpation
Lab ValuesLab ValuesNaNa++, K, K++, BNP, BUN/creatinine, BNP, BUN/creatinine
Intake and OutputIntake and OutputFluid & Sodium RestrictionFluid & Sodium Restriction
Urine Output & Daily WeightsUrine Output & Daily Weights
Heart FailureHeart FailureTeachingTeaching
Diet ModificationsDiet ModificationsRestricted Sodium IntakeRestricted Sodium Intake
Normal Fluid Intake (after stabilized)Normal Fluid Intake (after stabilized)
Medication RegimenMedication RegimenCommon Side EffectsCommon Side EffectsAdhering to RegimenAdhering to Regimen
Signs and Symptoms of HFSigns and Symptoms of HFMonitor Daily WeightsMonitor Daily Weights
EdemaEdemaShortness of BreathShortness of Breath
Nursing Interventions & ConsiderationsNursing Interventions & Considerations
Heart FailureHeart Failure
““Because multidrug regimens Because multidrug regimens are often necessary, patient are often necessary, patient
education is essential to limit education is essential to limit complications and complications and
hospitalizations that result hospitalizations that result from poor adherence to the from poor adherence to the
treatment regimen”treatment regimen”(Wynne, Woo, & Olyaei, 2007, p. 1009)(Wynne, Woo, & Olyaei, 2007, p. 1009)
Nursing Interventions & ConsiderationsNursing Interventions & Considerations
TJC Core TJC Core MeasuresMeasures
The Joint Commission defines Core The Joint Commission defines Core Measures as standardized performance Measures as standardized performance measures, with precisely defined data measures, with precisely defined data elements, calculation algorithms, and elements, calculation algorithms, and standardized data-collection protocols. standardized data-collection protocols. In other words, using Core Measures is In other words, using Core Measures is a way to find out if patients are getting a way to find out if patients are getting
good care. By requiring all good care. By requiring all organizations to use the same organizations to use the same
measures, TJC is leveling the playing measures, TJC is leveling the playing field so hospitals and clinicians have field so hospitals and clinicians have reliable data for self-assessment, as reliable data for self-assessment, as
well as benchmarks for comparisons. well as benchmarks for comparisons.
TJC Core MeasuresTJC Core Measures
Acute Myocardial InfarctionAcute Myocardial Infarction(AMI)(AMI)
Community Acquired PneumoniaCommunity Acquired Pneumonia(CAP)(CAP)
Surgical Care Improvement PlanSurgical Care Improvement Plan(SCIP)(SCIP)
Heart FailureHeart Failure (HF)(HF)
TJC Core MeasuresTJC Core Measures
LVF Assessment (echocardiogram)LVF Assessment (echocardiogram) ACEI or ARB for LVSD (EF < 40%)ACEI or ARB for LVSD (EF < 40%)
Adult smoking cessation Adult smoking cessation advice/counselingadvice/counseling
Discharge instructions include Discharge instructions include reconciliation of medication reconciliation of medication
regimenregimen
Heart FailureHeart Failure
ReferencesReferencesChojnowski, D. (2007). Protecting our patients from harm: Taking an Chojnowski, D. (2007). Protecting our patients from harm: Taking an
aim at heart failure. aim at heart failure. Nursing 2007, 37Nursing 2007, 37(11), 50-55.(11), 50-55.
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Moser, D. K., & Riegel, B. (2008). Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to Cardiac nursing: A companion to braunwald’s heart disease.braunwald’s heart disease. Saunders Elsevier: St. Louis, MO. Saunders Elsevier: St. Louis, MO.
Nolan, M. N. (2004). Nolan, M. N. (2004). JCAHO core measures. JCAHO core measures. Hoffman Estates, IL: Hoffman Estates, IL: Nursing Spectrum.Nursing Spectrum.
Skidmore-Roth, L. et al. (2007). Skidmore-Roth, L. et al. (2007). Mosby’s nursing drug reference, Mosby’s nursing drug reference, (20(20thth ed.). St. Louis, MS: Mosby Elsevier. ed.). St. Louis, MS: Mosby Elsevier.
ReferencesReferencesSmeltzer et al. (2008). Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-Brunner and suddarth’s textbook of medical-
surgical nursing, surgical nursing, (11(11thth ed.). Philadelphia, PA: Lippincott Williams ed.). Philadelphia, PA: Lippincott Williams and Wilkins.and Wilkins.
Vavouranakis, I., et al. (2003). Effect of home-based intervention on Vavouranakis, I., et al. (2003). Effect of home-based intervention on hospital readmission and quality of life in middle-aged patients hospital readmission and quality of life in middle-aged patients with severe congestive heart failure: A 12-month follow up study. with severe congestive heart failure: A 12-month follow up study. European Journal of Cardiovascular Nursing, 2European Journal of Cardiovascular Nursing, 2(2),(2), 105-111.105-111.
Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitioner prescribers, Pharmacotherapeutics for nurse practitioner prescribers, (2(2ndnd ed.). ed.). Philadelphia, PA: F. A. Davis Company.Philadelphia, PA: F. A. Davis Company.
http://www.pbm.va.gov/monograph/nesiritidemonograph.pdfhttp://www.pbm.va.gov/monograph/nesiritidemonograph.pdf