Pinoynursingbulletin providing you with an online nursing notes and solutions CONGESTIVE HEART FAILURE DESCRIPTION Congestive heart

failure (CHF) is the principal complication of heart disease. It is a pathophysiologic state produced by an abnormality incardiac pump function (either transient or prolonged). The heart is unable to transport blood in a sufficient flow to meet metabolic needs. CHF occurs at sometime in most cases of severe heart disease. This produces a variety of clinical circumstances fromacute left ventricular dysfunction (due to tachyarrhythmia,bradyarrhythmia, and acute myocardial infarction)to chronic left ventricular dysfunction (due to chronicvolume/pressure overload as seen in valvular heartdisease) Two physiologic components explain most of the clinical findings of CHF - most patients have findingsconsistent with both mechanisms: an inotropic abnormality resulting in diminishedsystolic emptying (systolic failure) a compliance abnormality in which the ability ofthe ventricles to accept blood is impaired (diastolicdysfunction). System(s) affected: Cardiovascular, Pulmonary Genetics: N/A Incidence/Prevalence in USA: Most commoninpatient diagnosis for patients over 65 Predominant age: Varies by etiology of heartdisease Predominant sex: Male > Female - ages 40-75 Male = Female - ages 75 and over SIGNS & SYMPTOMS Early and mild impairment: Dyspnea on exertion-cardinal sign of left heart failure Deteriorating exercise capacity Easy fatigue Difficulty breathing Weakness Moderate impairment: Nocturnal nonproductive cough Orthopnea Paroxysmal nocturnal dyspnea Wheezing, especially nocturnal in absence of historyof asthma or infection (cardiac asthma) Anorexia Fullness or dull pain in RUQ Tachypnea at rest Anxiety Hepatomegaly with tenderness to palpation Severe Cerebral dysfunction Abdominal bloating (ascites) Cyanosis www.pinoynursingbulletin.blogspot.com

Tachypnea with mild exertion Basilarrales Positive hepatojugular reflux Faint S3 gallop Nocturia

Cool extremities due to peripheral vasoconstriction Prominentrales over bases Right pleural effusion Edema Gallop rhythm Diastolic hypertension Elevated jugular venous pressure Cardiomegaly

impairment: Hypotension Pulsusalternans Anasarca Frothy and/or pink sputum

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Pinoynursingbulletin providing you with an online nursing notes and solutions Increased P2 Cardiac cachexia Cheyne-Stokes respirations

CAUSES Coronary artery disease Myocardial infarction Cardiomyopathy Alcoholic Viral Long-standing hypertension Drugs (e.g., chemotherapeutic agents) Muscular dystrophy Amyloidosis Postpartum state Valvular abnormalities Aortic stenosis or regurgitation Rheumatic heart disease (mitral and aortic valvulardisease) Renal artery stenosis, usually bilateral, may cause recurrent flash pulmonary edema Volume overload Cardiac depressants; negative inotropes (e.g., betablockers, IV amiodarone) Arrhythmias, eg, atrial fibrillation High output states Hyperthyroidism Beriberi heart disease HIV RISK FACTORS Iatrogenic reduction of intensity of therapy Inappropriate sodium and/or fluid excess Patient non-compliance Intercurrent arrhythmia, eg, atrial fibrillation Administration of drug with negative inotropic effects Excessive physical, emotional, or environmental stress Thyrotoxicosis, pregnancy, or any condition associatedwith increased metabolic demand Recent pregnancy (postpartum cardiomyopathy) DIAGNOSIS DIFFERENTIAL DIAGNOSIS Simple dependent edema Exertional asthma Severe diffuse CAD Occult COPD Nephrotic syndrome: excluded by absence of history of asymptomatic edema, proteinuria in nephrotic range,and history of renal disease Cirrhosis: excluded by absence of stigmata of liverdisease, and history of liver disease and its risk factors Left heart failure: findings of pulmonary congestion anddiminished cardiac output appearing in patients withmyocardial infarction, aortic and mitral valve disease,and hypertensive disease Right heart failure: findings of systemic vascularcongestion (edema, ascites) appear in patients with corpulmonale, tricuspid insufficiency, and most commonlyin patients with uncorrected prolonged left heart failure Venous occlusive disease with subsequent peripheraledema www.pinoynursingbulletin.blogspot.com

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LABORATORY B-type natriuretic peptide (BNP) is a marker of ventriculardysfunction; >100 is consistent with CHF. May behelpful in: Evaluating treatment since its value changes rapidly The emergency setting to help differentiate the cause of dyspnea Lab findings in early and mild to moderately severeCHF Respiratory alkalosis Mild azotemia Decreased erythrocyte sedimentation rate Proteinuria (usually less than 1 gm/24 h that clearswith treatment) Lab findings in severe CHF Increased creatinine Hyperbilirubinemia in severe cases Dilutionalhyponatremia Drugs that may alter lab results: N/A Disorders that may alter lab results: Renalfailure may elevate BNP PATHOLOGICAL FINDINGS Early and acute Firm lungs with microscopic revealing engorgedcapillaries with thickening of the alveolar septa withextravasation of red cells and edema fluid Liver is engorged, firm, and fluid-filled. Microscopic - reveals dilated central hepatic veins and sinusoids. Late and chronic Hemosiderin deposits in lungs Nutmeg liver with centrilobular necrosis Occasionallyhemorrhagic nonbacterial enterocolitiswith hemorrhagic necrosis secondary to mesentericvasoconstriction IMAGING X-ray - mild changes: pulmonary artery wedge pressure = 18-23 mm Hg (2.4-3.1 kPa) Increased heart size Increased blood flow to the upper lobes Equalization of flow between the upper and lowerlobes X-ray - moderate severe pulmonary artery wedge pressure= 20-25 mm Hg (2.7-3.3 kPa) Interstitialedema Kerley s B lines Perivascular edema Subpleural effusions X-ray - severe changes: pulmonary artery wedge pressure> 25 mm Hg (> 3.3 kPa) Alveolar edema Butterfly pattern of pulmonary edema

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Pinoynursingbulletin providing you with an online nursing notes and solutions DIAGNOSTIC PROCEDURES Echocardiographic studies are the most useful tests Cardiac catheterization, both right and left, for fulldiagnosis and prognosis B-type natriuretic peptide (BNP) is a useful marker ofventricular dysfunction. It is a cardiac neurohormonesecreted from the ventricles in an increasing amount inresponse to abnormal pressure overload and increasingvolume. The levels of BNP have been shown toincrease in patents in i correlation with progressiveworsening of NYHA class of congestive heart failure(CHF). B-type natriuretic peptide has been shown tobetter predict the presence or absence of CHF than anyset of clinical or lab measures of the cause of dyspnea. A level of over 100 is consistent with CHF. The levelchanges rapidly in response to treatment or worseningof the situation, so may be helpful not only in diagnosis but in following the benefit of treatment. It is helpfulin the emergency room to differentiate the cause ofdyspnea. Complete PFTs Nuclear imaging to evaluate LV and RV size andsystolic function

TREATMENT APPROPRIATE HEALTH CARE Inpatientwhen severe GENERAL MEASURES Immediate treatment of the heart failure Search for underlying correctable conditions Eliminate contributing factors when possible Supplemental oxygen Antiembolism stockings Fluid and sodium restriction. Education about this isimperative for long term control. Daily weights guideoverall therapy. Identify and control underlying correctable conditions(e.g., acute MI, valvular disease, hyperthyroidism, butmost commonly inadvertent salt and/or fl uid overload) SURGICAL MEASURES Heart valve surgery - possibly, if defective heart valveis responsible; mitral valve repair especially helpful ifmitral regurgitation is aggravating CHF Cardiac transplantation - to be considered in patients(age < 55) without other disqualifying medical problems,who are developing CHF unresponsive to othertherapeutic maneuvers, and who are felt to have a lifeexpectancy of less than a year Biventricular pacing ACTIVITY During severe stage, bed rest with elevation of headof bed and anti -embolism stockings to help control legedema Gradual increase in activity with walking will helpincrease strength DIET Sodium restriction (initially 4 gm sodium qd) Weight reduction diet if appropriate Low fat diet to retard coronary artery disease Appropriate fluid restriction

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MEDICATIONS DRUG(S) OF CHOICE Diuretics, usually in combination with dig italis areused to initiate therapy. ACE inhibitors have become amainstay of therapy. For acute pulmonary edema, IVmorphine remains cornerstone of therapy. Digoxin Improves contractility, slows ventricular rate in atrial fibrillation May be harmful in acute MI, hypertrophic cardiomyopathy,or aortic stenosis Loading dose should be sufficient to have early beneficial effect, especially in atrial fibrillation with a rapidrate, e.g., 0.5 -1.0 mg IV/PO, then another 1.0-1.5 mgin divided doses q4-6h Diuretics Furosemide (Lasix): IV or PO, depending on severityof pulmonary congestion. May require continuousdrip. Metolazone (Zaroxolyn): excellent addition whenfuros emide does not seem to be sufficient Spironolactone: when used ca refully, to avoid hyperkalemia. An important addition to difficult chroniccases. ACE Inhibitors Used to decrease afterload - shown to increase survival Improve general symptomatology and overall exercisecapacity Beta-blockers Carvedilol (Coreg) 3.125 mg po bid for 2 weeks, then6.25 mg bid for 2 weeks, increased to maximum 25mg bid for class I to III CHF Bisoprolol (Zebeta) 5-20 mg/day: in CIBIS-II study significantly decreases all-cause mortality and suddendeath ( treatment effects were independent ofthe severity or cause of heart failure ) Vasodilators IV nitroglycerin may be of short-term benefit to decrease preload, afterload, and systemic resistance. Oral medications, e.g., hydralazine, prazosin, andIsosorbidedinitrate demonstrate tachyphylaxis Contraindications: Refer to manufacturer s literature Precautions: ACE inhibitors may produce hypotension on First use in volume depleted patients. Betablockersmay produce profound hypotension. Significant possible interactions: Calciumchannel blockers may impair LV function especiallywhen used with beta blockers. Amlodipine seems lesslikely to be a problem. ALTERNATIVE DRUGS Sympathomimetic amines. Can be used in severe CHFunresponsive to above measures Dopamine and dobutamine have been successful forshort peri ods in treatment Dobutamine can be used on an intermittentoutpatient basis with intermittent infusion. However,in spite of possibly improving quality of life, reduces long-term survival.

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FOLLOWUP PATIENT MONITORING Variable depending on clinical circumstances. Initiallyevery 2-3 weeks after patient stabilized. Closely follow - history and physical fi ndings, chestx-ray, electrolytes, BUN, and creatinine PREVENTION/AVOIDANCE Treatment ofunderlying disorders when possible POSSIBLE COMPLICATIONS Electrolyte disturbance Atrial and ventricular arrhythmias Mesenteric insufficiency Protein enteropathy Digitalis intoxication EXPECTED COURSE/PROGNOSIS Result of initial treatment is usually good, whatever thecause Long-term prognosis variable. Mortality rates rangefrom 10% with mild symptoms to 50% with advanced,progressive symptoms. Killipclassification for heart failure Class Interpretation Mortality rate ------------------------------------I No CHF <5% II Mild-Moderate CHF 10% III Severe CHF 30% IV Cardiogenic shock >80% ------------------------------------bibasilarrales and/or S3 gallop rales over > 50% lung fi elds,S3 gallop, pulmonary edema BP <90 mm Hg (<12 kPa) with hypoperfusion, e.g., oliguria, confusion, clammy skin AGE-RELATED FACTORS Pediatric: Usually associated with congenital heartdisease Geriatric: Medications may need dosage adjustment Age-related cardiomyopathy is an increasing problem.It should be considered when the elderly complain ofunusual dyspnea or easy fatigue. Beta-blockers may beof help. Others: N/A PREGNANCY If occurs, will require special care SYNONYMS Heart failure Circulatory failure Dropsy Cardiac failure ABBREVIATIONS CCF = congestive cardiac failure

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