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HEART FAILURE NUR240 R. Kolk, revised 11/09 J. Borrero 1 Heart Failure • • • • Also called pump failure Left-sided heart failure Right-sided heart failure High-output failure 2 Etiology • Heart failure is caused by systemic hypertension in 75% of cases. • About one third of clients experiencing myocardial infarction also develop heart failure. • Structural heart changes, such as valvular dysfunction, cause pressure or volume overload on the heart. 3 Etiology • A syndrome of Pulmonary and/ or Systemic congestion due to C.O • Heart is unable to pump enough blood to meet tissues O2 requirements Pulmonary pressure fluid in alveoli (PULMONARY EDEMA) Systemic pressure fluid in tissues (PERIPHERAL EDEMA) 4 ETIOLOGY & RISK FACTORS Cardiac pathology that changes heart’s performance _____________________ _____________________ _____________________ _____________________ Risk Factors: 5 Compensatory Mechanisms • Sympathetic nervous system stimulation • Renin-angiotensin system activation • Myocardial hypertrophy 6 LOCATION Heart failure classified according to location of ventricular failure One ventricle may fail independently of another, but failure in one will impact on the other. L sided failure- pulmonary congestion R sided failure- peripheral congestion 7 Left-Sided Heart Failure • Manifestations include: – – – – – – – – – Weakness Fatigue Dizziness Confusion Pulmonary congestion Shortness of breath Oliguria Organ failure, especially renal failure Death 8 (L) SIDED HF Tissue hypoxia occurs because heart is unable to efficiently pump blood CLINICAL SIGNS of pulmonary congestion: Dyspnea Orthopnea Cough WT. gain Fatigue Anxiety/ restless S3 Cardiomegaly Crackles HR BP 9 Right-Sided Heart Failure • Manifestations include: – Distended neck veins, increased abdominal girth – Hepatomegaly (liver engorgement) – Hepatojugular reflux – Ascites – Dependent edema – Weight: the most reliable indicator of fluid gain or loss 10 (R) SIDED HF Blood “BACKS UP” into venous circulation. High oncotic pressure pushes fluids into tissues. CLINICAL SIGNS: CVP SUDDEN WT. GAIN JVD DEPENDENT EDEMA FATIGUE LIVER CONGESTION LETHARGY ASCITES ORTHOPNEA ANOREXIA 11 Assessments • Laboratory assessment- electrolytes, • BNP- B type natriuretic peptide. Normal =0 • Radiographic assessment • Electrocardiography • Echocardiography, TEE • Pulmonary artery catheters 12 Nursing Assessments • • • • • • O2 Saturation Vital Signs Heart Rhythm Lung Sounds Level of dyspnea Serum Electrolytes • • • • Daily weights Changes in LOC I&O Coping ability of pt and family • Signs of drug toxicity 13 GOALS Enhance O2 supply Work of heart by promoting contractility Interventions: 1. Adequate ventilation 2. Maintain cardiac function 3. Promote rest 4. Other 5. Medication 14 15 Nursing Interventions 1. ADEQUATE VENTILATION • • • Monitor respirations, breath sounds Administer O2 Position- high-Fowlers 16 Interventions 2. MAINTAIN CARDIAC FUNCTION • Monitor heart sounds • Pulmonary Artery Catheter Measurements CVP Pulmonary Artery Pressure Pulmonary Capillary Wedge Pressure Cardiac Output 17 Interventions 3. Promote rest until patient is stable strain on heart BR promotes cardiac efficiency Elevate legs to enhance venous return 18 Interventions 4. MISC. • Monitor LOC • Assess edema • Provide adequate nutrition • • Provide emotional support Maintain diet restrictions as prescribed (Na and fluid) 19 MEDICATION 5. • • • Medication Improve myocardial muscle function Restore C.O. & SV Reduce cardiac demands Natrecor (h BNP)- causes natriuresis in acute HF loss of Na and vasodilation B-type natriuretic peptide 20 MEDICATIONS • Fluid load, Preload, Afterload ACE inhibitors & Diuretics • Improve contractility Digoxin Dobutamine • Workload of the heart “Blockers” 21 Drugs That Enhance Contractility • Digitalis – Digitalis toxicity includes anorexia, fatigue, muscle weakness,changes in mental status. – Monitor heart rate for 1 full minute.Hold for <60 – Monitor electrolytes – Take same time each day • Other inotropic drugs including dobutamine, dopamine • Beta-adrenergic blockers 22 Improve contractility Inotropic agents Digoxin: cardiac glycoside • force of myocardial contraction & slows HR ( C.O. venous pressure, diuresis) • Narrow therapeutic range: – Monitor for toxicity – Digitalization: dobutamine, dopamine, milrinone (Primacor) 23 Advanced Calculations for IV Meds ordered/Kg/Minute 1. Convert to like units, such as mg to mcg or lb to kg 2. Calculate desired dosage per minute: mg/kg/min X kg = mg/min 3. Calculate the dosage flow rate in mL/min Dosage on hand = Dosage desired/min Amt solution on hand X amt desired/ min 4. Calculate the flow rate in mL/hour mL/min X 60 min/h = mL/hr 24 Homework 1.Dobutamine 250mg / 250 mL D5W to infuse at 5 mcg/kg/min. Weight- 80 kg Flow rate on pump2.Dopamine 800 mg/ 500 mL D5W to infuse at 4 mcg/kg/min. Weight- 190 lbs. Flow rate on pump25 Afterload Reducing Agents • ACE inhibitors-enalapril (Vasotec) captopril (Capoten) • Beta-blockers- carvedilol (Coreg) • metoprolol (Lopressor XL) • Angiotensin receptor II blockers losartan (Cozaar) • Nitrates- preload and afterload • 26 DIURETIC THERAPY Increases excretion of NA+/H2O/K Sites of action differ Result in varying degrees of ‘lyte imbalance Categories: Loop, Thiazide, K+-sparing 27 NURSING INTERVENTIONS DIURETIC THERAPY- give early in day • Monitor WT. • Assess for edema • Strict I&O • Monitor electrolytes • Nutrition = Low Na+ diet, K + supplements 28 LOOP DIURETICS MORE POTENT ACTION furosemide (LASIX) bumetamide (BUMEX) PO/ IV ACTION: at loop of Henle, K+ loss, Na+/Cl- excretion ADVERSE EFFECTS: orthostatic hypotension, may digitalis toxicity, hypokalemia Teach: K rich foods, po K, S&S hypokalemia 29 THIAZIDE DIURETICS Useful for maintenance • HCTZ (Hydrochlorothiazide) Action: excretion of Na+/Cl- & H2O Adverse effects: orthostatic hypotension, may digitalis toxicity 30 K+ Sparing Diuretics Maintenance therapy – conserves K+, has a gradual diuretic effect Spironolactone (Aldactone) Action: blocks reabsorption of Na+/ClAdverse effects: Hyperkalemia 31 Potential for Acute Pulmonary Edema due to Left Sided HF • Interventions include: – Assess for early signs, such as crackles in the lung bases, dyspnea at rest, tachycardia, disorientation, and confusion. – Productive cough of pink frothy sputum – Rapid-acting diuretics are prescribed, such as Lasix or Bumex. – IV morphine sulfate – Oxygen and/or intubation – Strictly monitor fluid intake and output. 32 PULMONARY EDEMA Rapid fluid accumulation in lung spaces that has leaked from engorged pulmonary capillaries Etiology – most common cause is sudden deterioration of LV function 33 Clinical signs • LV diastolic pressure pulmonary pressure • Lungs become “stiff” due to fluid buildup, resulting in hypoxia _________________ _________________ _________________ _________________ _________________ 34 Nursing Interventions • Administer O2 to relieve hypoxia & dyspnea • CPAP,PEEP • Assess breath sounds and monitor respirations • Pulmonary Artery Catheter • Hi fowler’s position • Urinary catheterization 35 Morphine Sulfate O2 demand, promotes peripheral vasodilation, relieves anxiety, CNS sedation Dose: up to 10 mg slow IV push Adverse effects: BP, respirations 36 Aminophylline Bronchodilator given to relieve wheeze/ bronchospasms that may occur IVPB loading dose, then IV continuous drip Monitor closely for adverse effects: GI upset, nervousness, HR, H/A, tremors 37 Cardiogenic Shock • Occurs with extensive LV injury perfusion to vital organs • Degree of shock, directly relates to level of ventricular failure • Results in: ______________ ______________ ______________ ______________ 38 Cardiogenic Shock Significant reduction in SV & CO causes drop in pressure & poor tissue perfusion a/r/o LV MI • Clinical signs: – BP, pulse, peripheral pulses – confusion/ agitation (cerebral hypoxia) – cold/ clammy skin – urine output – Resp distress – Chest pain 39 Treatment • • • • • • • Hemodynamic monitoring Reduce demand on the heart Improve oxygenation Improve tissue perfusion Intra-aortic balloon pump Inotropic Meds to BP, workload Correct underlying pathophysiology 40 NCLEX TIME The nurse is awaiting the arrival of a client from the ER who is being admitted with a LVMI. The nurse should be alert for which S&S of left-sided heart failure? A. Jugular vein distention B. Hepatomegaly C. Dyspnea D. Crackles E. Tachycardia 41 NCLEX TIME Harvey is a 76-year-old man being followed up by his nurse practitioner for congestive heart failure (CHF). Which assessment finding would be typically found in an older adult? • A.Orthostatic hypotension in conjunction with drug therapy for CHF • B.Clearing of crackles immediately after medication treatment • C.Auscultation of crackles • D.Digitalis toxicity 42 NCLEX TIME Carlos is prescribed digoxin after having open heart surgery and postoperative atrial fibrillation. Which statement, if made by the client, demonstrates the need for further teaching regarding his digoxin medication? • A.“I should notify my doctor if my pulse is less than 60 or more than 100 beats/min.” • B.“I need to keep my laboratory appointments.” • C.“I should not take my digoxin at the same time as antacids or laxatives.” • D.“If I forget to take my digoxin one day, I can double up on the dose the next day 43 NCLEX TIME • Mrs. Clark is an 83-year-old woman admitted with symptoms of heart failure. Her nurse, after performing the assessment, tries to decipher between right- and leftsided heart failure. Which symptoms below are consistent with left-sided heart failure? • A. Weight gain, jugular distention, and distended abdomen • B. Fatigue, weakness, and palpitations • C. Agitation, blood tinged, frothy sputum, dyspnea • D. Anorexia and nausea, distended abdomen, and enlarged liver 44 NCLEX TIME Provide the rationale Therapy for each of the O2 following therapies: Diuretics Rationale Bedrest Inotropic agents Vasodilators Fluid restriction Sodium restriction 45