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HEART FAILURE. NUR240 Lecture 4. Heart Failure. Also called pump failure Left-sided heart failure Right-sided heart failure High-output failure. Etiology. Heart failure is caused by systemic hypertension in 75% of cases.
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HEART FAILURE NUR240 Lecture 4 R. Kolk, revised 11/09 J. Borrero
Heart Failure • Also called pump failure • Left-sided heart failure • Right-sided heart failure • High-output failure
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.
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)
ETIOLOGY & RISK FACTORS Cardiac pathology that changes heart’s performance • _____________________ • _____________________ • _____________________ • _____________________ Risk Factors:
Compensatory Mechanisms • Sympathetic nervous system stimulation • Renin-angiotensin system activation • Myocardial hypertrophy
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
Left-Sided Heart Failure • Manifestations include: • Weakness • Fatigue • Dizziness • Confusion • Pulmonary congestion • Shortness of breath • Oliguria • Organ failure, especially renal failure • Death
(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 Crackles Cardiomegaly HR BP
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
(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
Assessments • Laboratory assessment- electrolytes, • BNP- B type natriuretic peptide. Normal =0 • Radiographic assessment • Electrocardiography • Echocardiography, TEE • Pulmonary artery catheters
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 Nursing Assessments
JCAHO Core Measures for HFEvery patient 100% of the time! HF-1: Written discharge instructions HF2: An evaluation of LVS function (Ejection fraction) HF3: ACE or ARB for LVS function HF4: Adult smoking cessation advice/counseling
GOAL Nursing Dx? Enhance O2 supply Work of heart by promoting contractility Interventions: • Adequate ventilation • Maintain cardiac function • Promote rest • Other • Medication
Nursing Interventions • ADEQUATE VENTILATION • Monitor respirations, breath sounds • Administer O2 • Position- high-Fowlers
Interventions • MAINTAIN CARDIAC FUNCTION • Monitor heart sounds • Pulmonary Artery Catheter Measurements CVP Pulmonary Artery Pressure Pulmonary Capillary Wedge Pressure Cardiac Output
Interventions • Promote rest until patient is stable strain on heart BR promotes cardiac efficiency Elevate legs to enhance venous return
Interventions • MISC. • Monitor LOC • Assess edema • Provide adequate nutrition • Provide emotional support • Maintain diet restrictions as prescribed (Na and fluid)
MEDICATION • Medication • Improve myocardial muscle function • Restore C.O. & SV • Reduce cardiac demands Natrecor (nesiritide)- Human B-type natriuretic peptide causes natriuresis in acute HF loss of Na and vasodilation
MEDICATIONS • Fluid load, Preload, Afterload • Improve contractility • Workload of the heart ACE inhibitors & Diuretics Digoxin Dobutamine “Blockers”
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
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)
Advanced Calculations for IV Meds ordered/Kg/Minute • Convert to like units, such as mg to mcg or lb to kg • 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
Homework 1.Dobutamine 250mg / 250 mL D5W to infuse at 5 mcg/kg/min. Weight- 80 kg Flow rate on pump- 2.Dopamine 800 mg/ 500 mL D5W to infuse at 4 mcg/kg/min. Weight- 190 lbs. Flow rate on pump-
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
DIURETIC THERAPY Increases excretion of Na+/H2O/K Sites of action differ Result in varying degrees of ‘lyte imbalance Categories: Loop, Thiazide, K+-sparing
NURSING INTERVENTIONS DIURETIC THERAPY- give early in day • Monitor WT. • Assess for edema • Strict I&O • Monitor electrolytes • Nutrition = Low Na+ diet, K + supplements
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
THIAZIDE DIURETICS Useful for maintenance • HCTZ (Hydrochlorothiazide) Action: excretion of Na+/Cl- & H2O Adverse effects: orthostatic hypotension, may digitalis toxicity
K+ Sparing Diuretics Maintenance therapy – conserves K+, has a gradual diuretic effect Spironolactone (Aldactone) Action: blocks reabsorption of Na+/Cl- Adverse effects: Hyperkalemia
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
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. • Rapid-acting diuretics are prescribed, such as Lasix or Bumex. • IV morphine sulfate • Oxygen and/or intubation • Strictly monitor fluid intake and output.
Clinical signs • LV diastolic pressure pulmonary pressure • Lungs become “stiff” due to fluid buildup, resulting in hypoxia • _________________ • _________________ • _________________ • _________________ • _________________
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
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
Cardiogenic Shock • Occurs with extensive LV injury perfusion to vital organs • Degree of shock, directly relates to level of ventricular failure • Results in: • ______________ ______________ • ______________ ______________
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
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
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? • Jugular vein distention • Hepatomegaly • Dyspnea • Crackles • Tachycardia
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
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
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 left-sided 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
NCLEX TIME Provide the rationale for each of the following therapies: