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199 Cards in this Set
- Front
- Back
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What are primary causes of heart failure?
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Hypertension, Coronary Artery Disease, myocardial infarction, rheumatic heart disease, congenital heart defects, pulmonary hypertension, cardiomyopathy, hyperthyroidism, valvular disorders, myocarditis
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What are precipitating causes of heart failure?
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anemia, infection, thyroid toxicosis, hypothyroidism, dysrhythmias, bacterial endocarditis, pulmonary embolism, paget's disease, nutritional deficiencies, hypervolemia
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What are contributing factors to the development of heart failure:
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diabetes, advanced age, tobacco use, obesity, high cholesterol, any conditions affecting cardiac output
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Inability of the heart to pump blood effectively
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Systolic heart failure
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Inability of the ventricles to relax and fill during during diastole
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diastolic heart failure
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What are signs and symptoms of right sided heart failure?
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right ventricular heaves, murmurs, jugular venous distention, edema (pedal, scrotum, sacrum), weight gain, increased heart rate, ascites, anasarca (massive generalized body edema), hepatomegaly (liver enlargement), fatigue, anxiety, depression, dependent bilateral edema, RUQ pain, anorexia, and GI bloating, nausea
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What are signs and symptoms of left sided heart failure?
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Left ventricular heaves, pulsus alternans (alternating pulses: strong, weak), increased heart rate, PMI displaced inferiorly and posteriorly (left ventricular hypertrophy), decreased PaO2 slight increase in PaCO2 (poor oxygen exchange), crackles (pulmonary edema), S3 and S4 heart sounds, pleural effusions, changes in mental status, restlessness, confusion, weakness, fatigue, anxiety, depression, dyspnea, shallow respirations up to 32-40 minute, paroxysmal nocturnal dyspnea, orthopnea, dry, hacking cough, nocturia, frothy pink tinged sputum (advanced pulmonary edema)
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What are some general signs of right sided heart failure (cor pulmonale)?
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-fatigue -increased peripheral venous pressure -ascites -enlarged liver and spleen -may be secondary to chronic pulmonary problems -distended jugular veins -anorexia and complaints of GI distress -weight gain -dependent edema |
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What are some general signs of left sided heart failure?
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-paroxysmal nocturnal dyspnea -elevated pulmonary capillary wedge pressure -pulmonary congestion: cough, crackles, wheezes, blood-tinged sputum, tachypnea -restlessness -confusion -orthopnea -tachycardia -exertional dyspnea -fatigue -cyanosis |
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Describe the general pathophysiology of right sided heart failure:
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Congestion of peripheral tissues leads to dependent edema and ascites, liver congestion: signs of impaired liver functions, and gi tract congestion: anorexia, GI distress, weight loss
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Describe the general pathophysiology of left sided heart failure:
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Leads to decreased cardiac output: activity intolerance and signs of decreased tissue perfusion, and pulmonary congestion: leads to impaired gas exchange: cyanosis and signs of hypoxia, and pulmonary edema: cough with frothy sputum, orthopnea, and paroxysmal nocturnal dyspnea
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This occurs when compensatory mechanisms maintain adequate cardiac output
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cardiac compensation
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This occurs when compensatory mechanisms can no longer maintain adequate cardiac output, resulting in inadequate tissue perfusion
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cardiac decompensation
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List and describe the cardiac compensatory mechanisms:
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-Sympathetic Nervous System Activation: increased release of catecholamines (epinephrine and norepinephrine) that results in increased HR, myocardial contractility, and peripheral vasoconstriction that initially improves cardiac output but increases the already failing heart's workload and oxygen demand, -Neurohormonal response: The RAAS, endothelin, and ADH promote sodium and water reabsorption, arterial vasoconstriction, and an increase in cardiac contractility and hypertrophy, Eventually this leads to ventricular remodeling which leads to increased ventricular mass, wall tension, oxygen consumption, and impaired contractility. It is a risk factor for life threatening dysrhythmias and sudden cardiac death. -Dilation: an enlargement of the chambers of the heart due to increased pressure from increased blood volume. Elastic elements of the muscle fibers are overstretched and can no longer contract effectively. -Hypertrophy: an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. Has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation, and is prone to dysrhythmias. |
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Describe the cardiac compensatory mechanism of SNS activation:
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increased release of catecholamines (epinephrine and norepinephrine) that results in increased HR, myocardial contractility, and peripheral vasoconstriction that initially improves cardiac output but increases the already failing heart's workload and oxygen demand,
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Describe the cardiac compensatory mechanism of neurohormonal response:
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The RAAS, endothelin, and ADH promote sodium and water reabsorption, arterial vasoconstriction, and an increase in cardiac contractility and hypertrophy, Eventually this leads to ventricular remodeling which leads to increased ventricular mass, wall tension, oxygen consumption, and impaired contractility. It is a risk factor for life threatening dysrhythmias and sudden cardiac death.
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Describe the cardiac compensatory mechanism of dilation:
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an enlargement of the chambers of the heart due to increased pressure from increased blood volume. Elastic elements of the muscle fibers are overstretched and can no longer contract effectively.
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Describe the cardiac compensatory mechanism of hypertrophy:
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an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. Has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation, and is prone to dysrhythmias.
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This involves inadequate pumping or filling of the heart. It is a syndrome not a disease.
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Heart failure
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Inability of the heart to pump blood effectively due to stretched and thin chambers often due to left ventricular hypertrophy with thick and stiffened chambers
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systolic heart failure
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What is normal ejection fraction? What does a decreased ejection fraction indicate?
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Normal= 55-65% EF <45% indicates left sided systolic failure. EF can go as low as 10% but ADLs are extremely difficult |
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What is the main cause of left sided heart failure?
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hypertension
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Cor pulmonale
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right sided heart failure
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What is the main clinical manifestation of acute decompensated heart failure?
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Pulmonary edema
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Describe the early stages of acute decompensated heart failure:
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mild increase in respiratory rate and decrease on PaO2
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Describe the progressive stage of pulmonary edema:
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-tachypnea and orthopne -SOB out of proportion to activity -lower PaO2 and increased PaCO2 -progressive respiratory acidosis -anxious, pale, possibly cyanotic -clammy and cold -respirations greater than 30 breaths per minute -orthopnea -crackles, wheezing, and maybe rhonchi -increased heart rate -blood pressure may be increased or decreased depending on the severity -cough with frothy, blood tinged sputum |
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What are late symptoms of pulmonary edema?
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decreased heart rate and blood pressure
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What does aldosterone do?
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cause sodium and water retention
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What are diagnostics for acute decompensated heart failure?
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-determine underlying cause -echocardiogram -nuclear imaging -chest x-ray -ECG -stress test -cardiac catheterization -O2 saturations, ABGs -serum electrolytes -B-type Natriuretic Peptide Level (BNP) |
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What is BNP?
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hormone produced by the heart muscle when volume and pressure increase inside the ventricle. Promotes venous and arterial dilation and increases preload. It is an antagonist to aldosterone.
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What are the levels of BNP that indicate normal or high probability of heart failure:
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<100= normal. heart failure is highly improbable 100-500= heart failure is probable >500= heart failure is highly probable |
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What is treatment for acute decompensate heart failure and the resultant pulmonary edema?
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-treat underlying cause -semi-Fowler's position, legs dangling or supine -inotropic drugs and diuretics -O2 per NC, mask, or BiPap, pulse oximetry, ABGs, monitor respiratory status -vitals -daily weights, I&O, monitor edema -urine output every hour -ECG -hemodynamic monitoring -mechanical ventilation -circulatory assist devices: intraaortic balloon pump and LVAC: left ventricular assist device (wear outside, battery operated, acts as a ventricle) |
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What is the recommended diet for ADHF?
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low sodium
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What are signs and symptoms of chronic heart failure?
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FACES -Fatigue: could be due to anemia -Limitation of Activities -Chest congestion/Cough: dry -Edema: peripheral, hepatomegaly, ascites and abdominal distention, pulmonary edema and pleural effusion, weight gain due to fluid retention may mask loss of muscle and adipose (due to anorexia), nocturia: blood flows better to kidneys when laying downs, sudden weight gain> 3lbs in 2 days= acute failure and need to call MD right away!!! -Shortness of breath/ dyspnea: ask number of pillows used for sleeping (orthopnea) -tachycardia (if on beta blockers may not see this): early sign of heart failure -skin changes: dusky, cool, damp, brown or brawny lower extremities -behavioral changes (due to decreased blood flow and oxygen to the brain): restlessness, unusual behavior, decreased attention span or memory, change in LOC/confusion. LATE SIGNS -chest pain: angina like pain and chest heaviness -dysrhythmias: Atrial fibrillation leads to clots leads to risk for stroke -renal failure: due to decreased blood flow |
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What is a diagnostic test for chronic heart failure?
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BNP (elevated)
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What are goals of treatment for chronic heart failure?
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-improve cardiac function -remove excess fluid and sodium -decrease cardiac demand -improve tissue oxygenation and decrease oxygen consumption |
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What are nutritional recommendations for chronic heart failure?
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-low sodium diet, restrict foods high in sodium -DASH diet -Weigh daily: same time daily, same scale, before breakfast, same type of clothing. Call if gained 3lbs over 2 days or 3-5lbs in 1 week -weight reduction |
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Describe treatment strategies for Heart Failure?
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Improve left ventricular function by: decreasing intravascular volume, decreasing venous return (preload), decreasing afterload, controlling heart rate and rhythm, improving gas exchange and oxygenation, increasing cardiac output, reducing anxiety, preserving target organ function, decreasing progression of the disease, possible inotropic agents.Treatment includes: oxygen therapy, diuretics, vasodilators including morphine, and possibly inotropic agents
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What are medications used to decrease intravascular volume? (heart failure)
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Diuretics= mainstay of treatment in volume overload -Loop -Thiazide -Potassium sparing -combination agents |
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What are the actions of diuretics and how are they administered?
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Enhance renal excretion of sodium and water. -increase urinary output -decrease circulating blood volume= decreased preload -decrease systemic and pulmonary congestion -decrease workload on heart Administered IV for acute CHF and orally for long term management |
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What are nursing care considerations for diuretic administration?
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-monitor weight (same time each day, similar clothing, on same scale); strict I&O -monitor blood pressure -watch for signs and symptoms of ototoxicity (furosemide IV given too quickly) and hypokalemia -photosensitivity (furosemide) is a problem for some, encourage sun block |
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What should you know about loop diuretics?
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Potent diuretics that increase urine output by preventing sodium, chloride, and water reabsorption in the loop of henle and distal tubule. Rapid acting when given IV. Side effects: Hypokalemia, hyperglycemia, and hyperuricemia Furosemide, ethacrynic acid, butemanide -furosemide IV push 20 mg over 1-2 minutes: too fast can cause deafness -take blood pressure prior to IV push: if <100 systolic question if it should be given; watch for hypotension -bumetanide= give IV |
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What should you know about thiazide diuretics?
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Increase in sodium, chloride, and water excretion by inhibiting reabsorption of sodium and chloride in the distal tubule; excretion of potassium in conjunction with sodium. Side effects: hypokalemia, hyperuricemia, hypercalcemia, hyperglycemia, and dermatologic reactions -chlorothiazide (often used with kids), hydrochlorothiazidem chlorthelidone, indapamide, metolazone -often 1st choice diuretic in chronic HF |
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What should you know about potassium sparing diuretics?
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-Spirinolactone: inhibition of action of aldosterone in distal tubule; increase sodium excretion and potassium retention side effects: hyperkalemia, gynecomastia, amenorrhea, GI disturbances; caution patients taking digoxin as increased potassium can decrease effects of digoxin Triamterene: unknown mechanism of action; action on distal tubule to cause sodium excretion and potassium retention Side effects: hyperkalemia, nausea and vomiting, leg cramps |
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What are combination diuretics and what should you know about them?
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Aldactazide (spironolactone and hydrochlorothiazide): more potent effect than single agents alone Side effects: GI disturbances, dizziness, and dry mouth Dyazide (triamterene and hydrochlorothiazide): potassium sparing effects Side effects: GI disturbances, dizziness, and dry mouth -Thiazides and loops often used together because they work on different sites in the kidneys therefore producing a synergistic effect |
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What are medications used to decrease venous return/ preload? (heart failure)
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Vasodilators: Nitroglycerin |
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What is the mechanism of action of medications used to decrease venous return/ preload?
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-Reduces amount of volume returned to left ventricle during diastole -can also be accomplished by positioning patient in a high fowler's position with feet horizontal in bed or dangling at the bedside. Decreases venous return due to pooling of blood in the extremities. Also increases thoracic capacity, allowing improved ventilation. |
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What should you know about nitroglycerin?
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Given IV in acute failure and pulmonary edema. -dilates arteries and veins, decreases preload and slightly reduces afterload (high doses) -increases blood to coronary arteries by dilating arteries -monitor blood pressure frequently (every 5-10 minutes when titrating) |
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What medications are used to decrease afterload and what is their mechanism of action? (heart failure)
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Nitroprusside, morphine, and nesiritide If afterload is decreased, cardiac output of the left ventricle improves, casing a decrease in pulmonary congestion |
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What should you know about nitroprusside?
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Given IV -potent vasodilator -dilates arteries and veins= reduces preload and afterload -drug of choice for ADHF and pulmonary edema because it has a rapid onset and potent effects on vascular system, myocardial contraction improves, increased cardiac output and decreased pulmonary congestion -Side effects: decreased blood pressure, thiocyanate toxicity: develops 49 hours after use. Headache, nausea, dizziness, dyspnea, blurred vision, sweating and restlessness. -monitor blood pressure frequently (every 5-10 minutes) during titration |
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What should you know about morphine?
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Often used with pulmonary edema and ADHF -decreases anxiety -decreases sympathetic stimulation -vasodilation of systemic and pulmonary blood vessels= increases venous pooling= decreases preload and afterload -dose= 1-2mg at a time to decrease preload -caution: monitor respiratory and blood pressure closely -use cautiously with acute failure |
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What should you know about nesiritide?
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Given IV -recombinant (synthetic) form of BNP and causes arterial and venous dilation: pools blood in the periphery -increased cardiac output without increase myocardial oxygen consumption or dysrhythmias -renal perfusion is enhanced -used in short term treatment of ADHF Side effects: decreased blood pressure, monitor blood pressure closely |
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What are medications used to improve heart muscle contractility?
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Digitalis glycosides (digoxin), Beta-adrenergic agonists (dopamine and dobutamine), phosphodiesterase inhibitors (inamirinone and milrinone)
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What is the action of digitalis glycosides (digoxin)?
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Positive inotrope. -increases myocardial contractility (increases force of contraction)= increased cardiac output, increased ejection fraction (% of blood emptied from the ventricle during systole; 60-70% in healthy heart but can be severely decreased in diseased heart). Unfortunately also increases myocardial oxygen consumption and is therefore only used when other medications not effective. -Reduces heart rate by slowing the rate of impulse through the conduction tissue (allows more time for filling of ventricles and enhances coronary circulation= decreased myocardial oxygen demand= decreases supply of oxygen and nutrients to the myocardium). Always take apical pulse for a full minute and if <60 hold the drug. -Slows the conduction of impulses through the AV node and purkinje fibers and increases the AV nodal refractory period. -Diuretic effect due to increased renal blood flow and filtration secondary to increased cardiac output |
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What is digoxin used for?
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-increases cardiac output in chronic CHF; not recommended for initial therapy in ADHF. Only use for short term treatment of ADHF, if other medications not working. -control atrial arrhythmias= slows transmission of impulses from atria protecting ventricles from over stimulation |
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What should you KNOW about therapeutic ranges for digoxin?
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It is commonly used. Use is limited because range between therapeutic and toxic doses is extremely narrow. Therapeutic range: 0.5-2ug/ml >2= toxic levels Kids= 0.8-2 WATCH for digoxin toxicity if potassium is <3.0mEq/L or magnesium is low |
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What is the usual dose of digoxin?
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0.125-0.25 mg a day. Available in elixir (clear green tinged liquid) form (0.05mg/ml). Infants- dose is calculated in micrograms. ALWAYS verify with another RN. If sending patient home with this, inform them to keep way out of reach of children and pets. |
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Describe administration and side effects of digoxin:
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Administration: IV given slowly over at least 5 minutes. IM not advised. Side effects: nausea, vomiting, anorexia, bradycardia, dysrhythmias, visual disturbances (yellow borders around dark objects, flickering lights, blurry vision) |
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Describe nursing care when giving digoxin:
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1. Take apical pulse for 1 minute immediately before giving the medication a. Adults: if pulse is less than 60/min= hold medicine & call physician b. Infants and young children: pulse less than 90-110/min= hold c. Older children: pulse <70/ min= hold d. Obtain a written order specifying the heart rate the drug should be withheld. 2. Caution: infants rarely receive more than 1ml (50ug or 0.05mg) in one dose; a higher dose is an immediate warning of an error. To ensure safety compare the calculation with another staff nurse. 3. Check potassium levels before giving (Normal= 3.5-5.0). Watch for hypokalemia (muscle weakness, depressed reflexes, anorexia, hypotension, paresthesia= abnormal sensation without cause, numbness, tingling) especially in patients taking furosemide. 4. Avoid sodium supplements because high in potassium, avoid licorice because it can cause water and sodium retention; avoid high sodium foods 5. Take 1 hour before or 2 hours after meals; do not give oral with meals having high fiber content. 6. Monitor I&O; weight changes (2lbs /day) and signs and symptoms of edema 7. Teach diarrhea and vomiting= alter electrolyte balance and can lead to digoxin toxicity 8. Teach to use special dropper that comes with the elixir. |
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What is the antidote to digoxin toxicity?
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digoxin immune FAB (digibind)
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What are examples of digitalis aminoglycosides?
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Digitoxin: long acting, slow onset, long half life; danger of accumulation toxicity is high!!! Digoxin: most commonly used; used rapid digitalization and maintenance therapy; rapid excretion |
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What is the mechanism of action of beta-adrenergic agonists and list some examples:
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Agonist= drug binds to receptor and stimulates receptor. -Stimulate beta adrenergic receptors causing increased contractility and increased heart rate Examples: -dopamine -dobutamine -epinephrine -norepinephrine |
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What are uses for beta-adrenergic agonists?
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-Short term treatment of ADHF in ICU and intermediate care with ECG monitoring -Role in long-term therapy is controversial |
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What are potential problems with long term treatment with beta adrenergic agonists?
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1. tolerance 3. increased ventricular irritability 3. increased need for oxygen by myocardium |
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What is the use, action, and important considerations for dopamine?
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Sympathomimetic; IV only. Use: severe ADHF, cardiogenic shock, hypotension and to increase heart rate in bradyarrythmias. Action: dose dependent Low doses: (2-5mcg/kg/min) vasodilates renal and mesenteric arteries, increasing blood to the kidneys (increases urine output) and decreases venous return (preload) and decreases workload and oxygen demand on the heart Moderate doses: (5-15mcg/kg/min) increases heart rate, increases contractility (increases cardiac output), decreases blood pressure High doses: (above 15mcg/kg/mi) are not beneficial due to vasoconstriction which occurs counteracting the positive effects of the drug. Can cause ventricular dysrhythmias. Extravasation can produce necrosis, monitor IV sight carefully to prevent necrosis Antidote: regitine |
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What is the use, action, and important nursing considerations for dobutamine?
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Selective beta-adrenergic agonist; IV only Sympathomimetic with beta one adrenergic activities. Use: to treat shock when increased cardiac output is needed Used often in "pump failure" because it is less likely to produce significant tachycardia and arrythmias than dopamine. Keep in mind, heart rate may increase with dobutamine, but not as significantly as with dopamine. This drug may be preferred over dopamine for short term treatment of ADHF. Action: increases myocardial contractility, stroke volume, and cardiac output with minimal increase in heart rate. (positive inotrope). Decreases systemic vascular resistance, Dose: 2-20mcg/kg/min |
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What is the action of phosphodiesterase inhibitors, list some examples and side effects:
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Action: Inodilator because they: increase myocardial contractility (+ inotrope) which leads to increased cardiac output. Promote peripheral vasodilation which decreases afterload. Examples: Inamrinone and milrinone. Some studies show inamrinone to be superior to dopamine or dobutamine. Side effects: dysrhythmias, thrombocytopenia, and hepatotoxicity. |
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Why is it important to improve oxygenation with heart failure?
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Oxygen therapy relieves dyspnea and fatigue. Rest is also very important.
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What is the action and route of ACE inhibitors?
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Action: Inhibits the normal function of the renin-angiotensin system in the kidneys. Blocks the conversion of angiotensin I to angiotensin II, resulting in: 1. vasodilation- (angiotensin II is a potent vasoconstrictor) 2. reduced water and sodium reabsorption: inhibits aldosterone secretion (normal causes sodium retention) 3. the above results in: decreased pulmonary and systemic vascular resistance, decreased blood pressure, and reduction in afterload and preload; increase blood flow to kidneys= promote natural diuresis Route: IV or oral |
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What are uses for ACE inhibitors?
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-Antihypertensive -CHF: used with digoxin and diuretics (caution because can potentiate effects of ACE inhibitor: hypotension= monitor carefully) -Post-MI with left ventricular dysfunction -diabetic neuropathy |
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What are side effects of ace inhibitors?
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-dry cough -headache -diarrhea -loss of taste -weakness -nausea -dizziness -hypotension -rash -fever -joint pain -angioedema of face, lips, tongue -renal dysfunction -hyperkalemia |
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What is nursing care associated with ACE inhibitors (prils)?
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-monitor blood pressure: especially after first dose; blood pressure can fall dramatically 1-3 hours after receiving especially those on sodium restricted diets, diuretics, or dialysis -avoid salt substitutes= high in potassium -monitor potassium and sodium levels -teach: report side effects and importance of compliance. Taste impairment generally disappears in 2-3 months. Some are affected by food, inform: captopril, moexipril, quinapril, and Ramipril have reduced absorption with meals. -Caution CHF patients to increase their physical activity slowly in response to the decreased chest pain. |
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What ACE inhibitors are used to treat CHF? Which are used in pediatrics to treat CHF?
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Captopril, enalapril, and lisinopril pediatrics= captopril and enalapril |
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Action, use, and examples of Angiotensin II receptor blockers
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Action: bind to angiotensin II receptor sites, preventing vasoconstriction and the aldosterone-secreting effects of the angiotensin II; affecting the site of action of angiotensin II not it's production. Outcome similar to ACE inhibitors. Use: When patient's cannot tolerate ACE inhibitors Examples: losartan and valsartan Dopamine: low doses= vasodilation renal circulation= increased urine output; moderate= increased heart rate, increase myocardial contractility, increased blood pressure (increases systemic resistance) |
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What is the action and use of beta-adrenergic blockers?
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Action: Block negative effects of SNS on failing heart ie, blocks increased heart rate. Use: Increased survival in heart failure has been shown with the use of beta-blocker, especially carvedilol and metoprolol; recommended to be used with other therapies |
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What at side effects and major side effects of beta-adrenergic blockers?
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side effects: can decrease myocardial contractility, therefore start gradually (increase dose slowly every 2 weeks) major side effects: edema, worsening heart failure, decreased blood pressure, fatigue, bradycardia |
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What should you know about specifically with carvedilol?
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1. Overdose= profound bradycardia, decreased blood pressure, bronchospasms, cardiogenic shock 2. Assess blood pressure and pulse at beginning of treatment and every 4 hours, <60= hold 3. Avoid abrupt withdrawal which can lead to sweating, palpitations, headache |
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What should you know about combination vasodilators used to treat heart failure?
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Isosorbide dinitrate/hydralazine: use only approved for African americans with chronic heart failure Isosorbide dinitrate: works to relax the veins and arteries Hydralazine: relaxes arteries and decreases the workload of the heart Common side effects: headache and dizziness Assess blood pressure and hold if systolic <90 |
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What are adjunctive pharmacologic agents and interventions for heart failure?
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Foley for accurate I&O Anticoagulants: for patient with history of emboli, recent onset of atrial fibrillation or existing left ventricular thrombi. Warfarin long term to maintain INR 2-3 |
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What are treatments for heart failure?
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-cardiac resynchronization therapy (CRT): biventricular pacemakers -cardiac transplants -mechanical options -intraaortic balloon pumps: assists increase of cardiac ouput: goes into aorta and inflates during diastole to displace the blood above the balloon to get better output which leads to better perfusion of coronary arteries. Contracts during systole and pulls back. -ventricular assist devices: up to 2 years |
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What should you teach heart failure patients about medications?
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-will take medications for the rest of their lives -expected actions and signs of drug toxicity with medications -how to take a pulse and what to reports -signs and symptoms of hypokalemia and hyperkalemia -blood pressure monitoring -when on digoxin and beta-adrenergic blockers teach to take pulse and call if <60 |
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What should you teach heart failure patients about dietary therapy?
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-written plan -how to read labels for sodium -DASH -no added salt -daily weights -smaller, more frequent meals |
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What should you teach heart failure patients about activity/rest?
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-Energy conserving and energy efficient behaviors -exercise training (cardiac rehabilitation) -increase gradually -avoid heat and cold extremes -rest after exertion -avoid emotional upsets |
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What should you teach about ongoing monitoring for heart failure patients? |
-know FACES -reappearance of symptoms -what to report -regular follow-up -support group -health promotion -vaccinations -reduce risk factors |
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Describe patient and family instructions for heart failure:
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Health promotion: 1. Obtain an annual flu vaccination 2. Obtain the pneumococcal vaccine and revaccination after 5 years (if you are at high risk of infection or serious disease) 3. Consider smoking cessation and weight reduction, if appropriate. Rest 1. Plan a regular daily rest and activity program 2. After exertion, such as exercise and ADLs, plan a rest period. 3. Shorten working hours or schedule rest periods during working hours 4. Avoid emotional upsets. Discuss your concerns, fears, feelings of depression, etc. with your health care provider. Drug Therapy 1. Take each drug as prescribed daily. 2. Develop a check-off system (daily chart or pill organizer) to ensure that your medications have been taken. 3. Take your pulse rate each day before taking your medications. Know what range your provider wants for your heart rate. 4. Learn to take your own blood pressure at determined intervals. Know you acceptable blood pressure limits. 5. Be alert for dizziness and light-headedness when changing positions or getting out of bed. Change positions slowly to prevent dizziness. 6. Watch for signs of internal bleeding (such as unusual pain in your joints or abdominal pain), bleeding gums, increased bruises, and blood in your stool or urine, and know what to do if you take anticoagulants. 7. Know your own international normalized ratio if you take Coumadin, and how often you are to have your blood checked. Dietary therapy 1. Refer to the written diet plan and list of permitted and restricted foods. 2. Examine food and drink labels to determine sodium content. Also, check for the sodium content of OTC medicines, such as laxatives, cough medicines, and antacids, 3. Avoid using salt when preparing foods, or adding salt to foods. 4. Weigh yourself in the early morning after arising and emptying your bladder. Use the same scale and wear the same or similar clothing every day. 5. Report a weight gain of 3lb in 2 days or 3-5bs in a week. 6. Eat smaller, more frequent meals. Activity program 1. Increase walking and other activities gradually, provided they do not cause fatigue and shortness of breath. Consider cardiac rehabilitation program. 2. Avoid extremes of heat and cold. 3. Keep regular appointments with your health care provider. Ongoing monitoring 1. Know the signs and symptoms of recurring or progressing heart failure, such as increased shortness of breath, increased swelling of your feet, rapid weight gain, or awakening at night unable to breath. 2. Recall the symptoms experienced when your illness began; reappearance of previous symptoms may indicate a recurrence. 3. Report immediately to your health care provider any of the following: -difficulty breathing, especially with exertion or lying flat -waking up breathless at night -frequent dry, hacking cough, especially when lying down -fatigue, weakness -swelling of ankles, feet, or abdomen: swelling of face or difficulty breathing (ACEs) -nausea with abdominal swelling, pain, and tenderness -dizziness and fainting -weight gain of 3lb in 2 days or 3-5lbs in a week 4. Follow up with your health care provider on a regular basis 5. Consider joining a local support group with your family members and or support person |
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What is cardiomyopathy?
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A structural or functional abnormality of the myocardium not related to cerebrovascular disease
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Describe myocarditis:
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-Inflammation of the myocardium (heart muscle) -can be acute or chronic -can occur at any age |
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How does myocarditis develop?
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-any viral infection (usually the cause and self-limiting if viral) -leads to necrosis of cardiac tissue -undamaged fibers hypertrophy (cardiomegaly) -causes loss of elasticity, impaired conduction, CHF, dysrhythmias -bacterial strep, rheumatic fever -autoimmune disease (diphtheria) -parasitic infection (toxoplasmosis) -less common: exposure to radiation, chemotherapy, other drugs, and chemicals |
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What is the prognosis for myocarditis?
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-the disease course depends on the size, number, and location of lesions -some respond well to treatment with no residual effects -others progress to cardiomyopathy and die |
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What are clinical manifestations of myocarditis?
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-nonspecific and vague signs and symptoms -fatigue -dyspnea -palpitations -fever -CHF and cadiomegaly -tachycardia -history of febrile episode, respiratory infection, or viral pharyngitis |
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What are diagnostic studies for myocarditis?
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-increase in antibody titers -nonspecific EKG changes, SVT, dysrhythmias |
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What is treatment for myocarditis?
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-cure infection: antibiotics, antipyretics -decrease cardiac workload: bed rest (usually hospitalized a long time) -O2 -Sodium restriction -medications such as diuretics, digitalis (based on symptoms) -detect life threatening arrhythmias and treat |
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Inflammation of the pericardium with thin strands of fibrinous exudate that extends from the epicardial surface to the pericardial sac.
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Pericarditis
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Describe pericarditis:
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Heart is enclosed in pericardial sac composed of 2 surfaces: the visceral and parietal sac -inflamed pericardium may result in localized or generalized deposits of fibrin which can produce constrictive pericarditis leading to a rigid and stiff pericardium which leads to decreased filling that can lead to eventual cardiac tamponade and decreased cardiac output |
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Describe the progression of pericarditis:
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-potential space between the parietal and visceral layers fill with fluid and pericardial effusion or tamponade may occur -compression on heart occurs due to increased fluid or fibrosis therefore leading to decreased filling of the heart -tamponade is due to increased fluid between pleuras and pressure put on heart restricting ventricular filling leading to cardiac emergency |
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Describe the etiology of pericarditis:
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-bacterial infection -viral infection -cardiac injury -uremia -trauma -autoimmune (dressler's syndrome) |
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Describe the different types of pericarditis:
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-Constrictive pericarditis -Post myocardial infarction pericarditis -Dressler's syndrome: weeks to months after MI, causes fever, pleuritic, and pericardial inflammation -Post cardiotomy syndrome Acute: lasting less than 6 weeks SubAcute: lasting 6 weeks to 6 months Chronic: lasting longer than 6 months |
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What is MAZE surgery?
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ablation therapy for atrial fibrillation
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What are the 3 main signs and symptoms of pericarditis?
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-pericordial pain -pericardial rub: grating, scratchy, scraping heart sounds -dyspnea |
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Describe the pericordial pain associated with pericarditis:
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-varies in intensity -characteristically sharp and stabbing -localizes to left and right shoulder, arm, elbow, and neck -pain tolerance varies with the patient -usually aggravated by breathing, turning in bed, or lying on left side, or coughing -pain relieved by sitting up -pain may be referred to right side of chest, epigastric region, trapezius ridge, substernal, or precordial and left nipple -most pain originates from inflammation of the diaphragm or diaphragmatic pleura. In the pericardium itself, only the lower part of the parietal pericardium senses pain -important to differentiate from MI pain |
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Describe the pericardial rub associated with pericarditis:
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-heard when epicardial surfaces lose lubricating fluid because of inflammation and pericardial and epicardial layers rub against each other -Doesn't radiate!! Whereas murmurs do. |
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Describe the dyspnea associated with pericarditis:
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-due to compression of bronchi or lung parenchyma by distended pericardium -patient gets some relief from dyspnea and pain by sitting up and leaning forward. (Dos not apply for MI pain and dyspnea so KEY to know this) -may accompany chest pain |
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What are diagnostic tests for pericarditis?
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-serial EKG's may help differentiate acute MI from pericarditis -CXR and echocardiogram used to identify pleural effusion -cardiac enzyme tests: CPK-MB may be elevated -increased sedimentation rate -increased leukocytosis: increased WBCs |
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Describe treatment for pericarditis:
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-relieve pain with NSAIDS such as aspirin or indomethacin. -corticosteroids for short time -antibiotics for bacterial pericarditis -CONTROL CAUSE -prevent complications: rest until fever and pain gone, treat signs and symptoms -pericardiocentesis: removal of fluid from pericardial sac through a needle/catheter -pericardiectomy: removal of parietal and/or visceral layers of pericardium may be necessary |
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Describe nursing care for pericarditis:
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-assess for pain -position to alleviate pain: upright sitting and leaning forward -bed rest while pain and/or friction exists -assess vitals q4h |
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What are potential complications for pericarditis?
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-Pericardial effusion: muffled heart tones, paradoxical pulse, decreased cardiac output, distended neck veins, diastolic pressure decrease -Cardiac tamponade: increased heart rate, decreased blood pressure: place in low fowlers to decrease pressure on the heart, give O2, and prep for pericardiocentesis -Chronic pericarditis: +progresses to constrictive pericarditis +due to scarred and rigid sac +effusive constrictive pericarditis due to thickened visceral pericardium, effusion between the visceral and parietal layers +adhesive pericarditis, entire pericardium and adjoining mediastinal structures involved |
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Describe infective endocarditis:
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-infection of the inner layer of heart, including the cardiac valves -improved prognosis with antibiotic therapy -10,000 to 15,000 new cases each year -acute or subacute (pre-existing valve conditions and can develop over several months) |
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Describe the etiology of infective endocarditis:
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-bacterial origin most common (streptococcus viridans or staphylococcus aureus) -viruses -fungi -IV drug abuse WOccurs when blood turbulence within heart allows causative organism to infect previously damaged valves or other endothelial surfaces |
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What are risk factors for infective endocarditis?
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-Cardiac, noncardiac, procedural -Principal risk factors include: age, IV drug abuse, prosthetic valves, use of intravascular devices, renal dialysis |
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Describe the vegetation associated with infective endocarditis
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-fibrin, leukocytes, platelets, and microbes -adhere to the valve or endocardium -parts break off and enter circulation (embolization) |
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What are clinical manifestations of infective endocarditis?
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-nonspecific -low-grade fever occurs in 90% of patients -chills -weakness -malaise -fatigue -anorexia -mumur in most patients (aortic and mitral valves most affected) -heart failure -Manifestations secondary to embolism: spleen= sharp RUQ pain, enlarged and tender, abdominal rigidity Kidneys= hematuria, pain, renal failure, watch output Limbs= ischemia or gangrene from emboli Brain= hemiplegia, aphasia, ataxia, change in LOC Lungs= pulmonary embolism |
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What are clinical manifestations of the sub-acute form of infective endocarditis?
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-arthralgias -myalgies -back pain -abdominal discomfort -weight loss -headache -clubbing of fingers |
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What are vascular manifestations of infective endocarditis?
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-splinter hemorrhages in nail beds -petechiae -Osler's nodes on fingers or toes (painful tender red purple pea sized lesions on fingertips or toes) -Janeway's lesions on palms or soles (flat painless red spots) -Roth spots (hemorrhages in the retina) |
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What are Osler's nodes?
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Painful tender red purple pea sized lesions on fingertips or toes associated with infective endocarditis
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What are Janeway's lesions?
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Flat, painless, red spots found on palms and soles of feet associated with infective endocarditis
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What are roth spots associated with infective endocarditis?
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hemorrhages in the retina
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What are diagnostic studies for infective endocarditis?
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-History: recent dental work, invasive urology, surgeries, gynecological exams, procedures, delivered a baby, dialysis, infection, invasive devices -Laboratory tests: +Blood cultures: 2 within 30 minutes from different sites, if has been on antibiotics may not grow right away so keep for a few weeks to see if it grows +CBC with differential: increased WBC +ESR, C-reactive protein: increased -echocardiography -CXR -ECG -Cardiac catheterization |
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What are the three main criteria for diagnosis of infective endocarditis?
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-positive blood culture -new or changed heart murmur -vegitations seen on echocardiogram |
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List target groups for antibiotic prophylaxis to prevent endocarditis:
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People with the following heart conditions should receive prophylactic antibiotics when they have certain conditions or procedures: -Congenital heart disease: +unrepaired cyanotic CHD (including palliative shunts and conduits) +repaired congenital heart defect with prosthetic material or device for 6 months after the procedure +repaired CHD with residual defects at the site or adjacent -cardiac transplantation recipients who develop heart valve disease |
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List the conditions or procedures requiring antibiotic prophylaxis in certain target groups to prevent infective endocarditis:
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When the target groups have the following conditions or procedures, they need prophylactic antibiotics: -Oral: +dental manipulation involving the gums or roots of the teeth +dental manipulation involving puncture of the oral mucosa +dental extractions of implants +prophylactic teeth cleaning with expected bleeding -Respiratory: +respiratory tract incisions (e.g. biopsy) +tonsillectomy and adenoidectomy -Gastrointestinal and genitourinary: +wound infection +urinary tract infection |
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Describe collaborative care for infective endocarditis:
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-Prophylactic antibiotic treatment for select patients having: certain dental procedures, respiratory tract incisions, tonsillectomy and adenoidectomy, GI wound infection, urinary tract infection -accurate identification of organism (one of main causes is strep infection) -IV antibiotics (long-term) -Repeat blood cultures -valve replacement if needed -antipyretics for fever -fluids -rest -if fungal: may need valve replacement |
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List subjective data collected in a nursing assessment of infective endocarditis:
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-Health history: +valvular, congenital, or syphillic cardiac disease +previous endocarditis +staph or strep infection -Drugs -Recent surgeries and procedures: anything invasive -IVDA -alcohol abuse -weight changes -chills -hematuria -exercise intolerance, weakness, fatigue -cough, DOE, orthopnea, palpitations -night sweats -pain, headache, joint or muscle tenderness |
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List objective data collected in a nursing assessment of infective endocarditis:
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-fever -Osler's nodes -splinter hemorrhage -Janeway's lesions -petechiae, purpura -peripheral edema, clubbing -tachypnea, crackles -dysrhythmias, tachycardia, murmur, s3, s4 -retinal hemorrhages |
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Describe health promotion for infective endocarditis:
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-identify those at risk -assess history and understanding of disease process -teach importance of adherence to treatment regime -patient teaching: +stress need to avoid infectious people +avoidance of stress and fatigue +rest +hygiene +prophylactic antibiotics +drug rehabilitation |
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Describe ambulatory and home care for infective endocarditis:
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-antibiotic therapy for 4-6 weeks -assess home setting -monitor laboratory data, including blood cultures -assess IV lines -coping strategies -adequate rest -moderate activity -compression stockings, ROM exercises, and deep breathe and cough every 2 hours to prevent blood clots and pneumonia |
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What is patient teaching for infective endocarditis?
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-monitor body temperature -signs and symptoms of complications -nature of disease and reducing risk of reinfection -stress follow up care, good nutrition, early treatment of common infections -signs and symptoms of infection -need for prophylactic antibiotic therapy |
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atrioventricular valves
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mitral and tricuspid
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semilunar valves
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aortic and pulmonic
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The types of valvular heart disease depend on what?
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-valves affected -type of functional alteration: +stenosis: narrowing or constricting +regurgitation: incompetent of insufficient and does not close completely |
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Describe heart valve stenosis:
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Constricting/narrowing -valve orifice is smaller -forward blood flow is impeded -pressure differences reflect the degree of stenosis |
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Describe heart valve regurgitation
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Incompetence/insufficiency -incomplete closure of valve leaflets -results in backward flow of blood |
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Describe mitral valve stenosis:
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-Majority of adult cases result from rheumatic heart disease +scarring of valve leaflets and chordae tendonae (rheumatic endocarditis) +contractures develop with adhesions between commissures of the leaflets -results in decreased blood flow from left atrium to left ventricle -increased left atrial pressure and volume -increased pressure in pulmonary vasculature -risk for atrial fibrillation |
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What are clinical manifestations of mitral valve stenosis?
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-exertional dyspnea due to decreased lung compliance -loud s4 -murmur -fatigue -palpitations -hoarseness -hemoptysis -chest pain, seizures/stroke |
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In mitral valve regurgitation, valves function depends on what?
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intact: -mitral leaflets -mitral annules -chordae tendinae -papillary muscles |
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In mitral valve regurgitation, what is the initial damage caused by?
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-MI -chronic rheumatic heart disease -mitral valve prolapse -ischemic papillary muscle dysfunction -Infective endocarditis |
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Describe mitral valve regurgitation
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-incomplete valve closure -backward flow of blood -acute mitral regurgitation: pulmonary edema -chronic mitral regurgitation: left atrial enlargement, ventricular hypertrophy (leads to decrease in cardiac output) |
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What are acute clinical manifestations of mitral valve regurgitation?
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-thread peripheral pulses and cool, clammy extremities -murmur |
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What are clinical manifestations of chronic mitral valve prolapse:
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-asymptomatic for years until development of some degree of left ventricular failure -weakness, fatigue, palpitations, progressive dyspnea -peripheral edema, s3, murmur |
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Describe mitral valve prolapse:
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-abnormality of mitral valve leaflets and the papillary muscle or chordae tendinae -leaflets prolapse back into left atrium during systole -usually benign with valve closing effectively -potential complications -unknown cause but genetic link in some |
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What are diagnostic studies for valvular heart disease?
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-patient's history/physical exam -CT scan of chest -echocardiogram -CXR -ECG -cardiac catheterization |
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What is conservative management of valvular heart disease?
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-prophylactic antibiotic therapy to prevent recurrent rheumatic fever and infective endocarditis -dependent on valve involved and disease severity -prevent exacerbations of heart failure, pulmonary edema, thromboembolism, and recurrent endocarditis -drugs to treat/control heart failure: vasodilators (nitrates, Aces), positive inotropes (digoxin), diuretics, and beta blockers -sodium restriction -anticoagulation therapy -antidysrhythmia drugs |
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Describe percutaneous transluminal balloon valvuloplasty for valvular disorders:
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-splits open fused commissures -for mitral, tricuspid, and pulmonic stenosis -balloon tipped catheter inserted via femoral artery -inflated to separate valve leaflets |
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Describe surgical therapy for valvular disorders
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Valve repair: -surgical procedure of choice -lower mortality -may not restore total valve function Valve replacement |
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Describe the different types of surgical valve repair:
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Commissurotomy (valvulotomy): -can be closed or open (more common) Valvuloplasty: -open (suture of torn leaflets) -minimally invasive Annuloplasty -reconstruct part of the valve |
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Describe the different types of valve replacement:
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Mechanical (artificial) (carbon, dacron, or metal) -last longer -risk of thromboembolism -require long-term anticoagulation Biologic (tissue) -bovine, porcine, or human -no anticoagulation required -less durable |
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Describe subjective data obtained in assessment of valvular disorders:
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-past medical history -IV drug abuse -fatigue -palpitations, weakness, activity intolerance, dizziness, faintaing -DOE, cough, hemoptysis, orthopnea, paroxysmal nocturnal dyspnea -angina or atypical chest pain |
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Describe objective data obtained in assessment of valvular disorders:
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-s3 and s4 -dysrhythmias -increase or decrease in pulse pressure; hypotension -thread peripheral pulses -hepatomegaly, ascites -weight gain, unexplained |
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Describe health promotion in valvular disorders:
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-diagnosing and treating streptococcal infection -prophylactic antibiotics for patients with history -encourage compliance -teach patient when to seek medical treatment -individualize rest and exercise -avoid strenuous activity -discourage tobacco use -ongoing cardiac assessments to monitor drug effectiveness -monitor INR |
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Describe patient teaching in valvular disorders:
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-drug actions and side effects -importance of prophylactic antibiotic therapy -information related to anticoagulation therapy -when to seek medical care -follow up care -medical alert bracelet |
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Describe rheumatic fever:
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-inflammatory disease that affects the heart, joints, CNS, and subcutaneous tissue -most significant sequel to rheumatic fever is rheumatic heart disease which causes damage to and scarring of mitral valve -on decline over past 30 years; although there have been recent outbreaks |
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Describe etiology of rheumatic fever:
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-Autoimmune process -Strep releases proteins and antibodies are formed -starts with pharyngitis (sore throat) Increased occurrence: -school age -low socioeconomic standard of living -crowded housing -cold, humid climate -parental or personal history of rheumatic fever -most have previous infection with beta hemolytic streptococci (2-6) weeks |
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What are clinical manifestations of rheumatic fever?
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-migratory polyarthritis (joints enlarged and painful) -carditis (inflammation of all parts of the heart, primarily mitral valves) -chorea (aimless shaking, involuntary movements of extremities and face that affects speech) - erythema marginatum (wavy edged rash/ red skin lesions starting on trunk and spreading peripherally) -subcutaneous nodules (small nontender swellings often over the joints) -fever with history of sore throat -abdominal pain occurs in some cases |
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Describe diagnostic evaluation of rheumatic fever:
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-no specific test -combination of signs and symptoms and lab findings -Jone's criteria: 2 major manifestations or 1 major and 2 minor manifestations -lab values: increased antistreptolysin-o ASO titers most reliable; 80% rheumatic fever indicates development of group A strep antibodies due to infection |
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Describe Jone's criteria for diagnosing rheumatic fever:
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2 major manifestations or 1 major and 2 minor manifestations Major manifestations= -arthritis -carditis -chorea Minor manifestations= -low grade fever, usually spiking in late afternoon -epistaxis -arthralgia -migratory polyarthritis -subcutaneous nodes -erythema marginatum |
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What are nursing interventions for rheumatic fever?
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-explain importance of ongoing longterm health supervision -need for antibiotic prophylaxis for dental work, infection, and invasive procedures -encourage adequate rest and nutrition to support body's natural defenses -administer salicylates to control inflammatory process and reduce fever and discomfort |
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What is treatment for rheumatic fever?
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-administer penicillin, check for allergies -prednisone -if carditis is present, explain any activity restrictions and help them choose less strenuous activities -stress that chorea is involuntary, transitory, and that all manifestations eventually disappear |
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Explain the difference between congenital and acquired heart defects:
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Congenital= present at birth; structural defects due to deviation or incomplete development; cause usually not known Acquired= due to some disease process affects the functioning of the heart; common is carditis due to strep infection or rheumatic fever and subsequent valvular stenosis BOTH lead to CHF |
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Describe some basic hemodynamic principles of the heart
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Pressure in the left side of the heart is greater than in the right side of the heart. Blood flows from areas of higher pressure to lower pressure.
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Describe and list acyanotic heart defects
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Conditions that result in: Increased pulmonary blood flow= atrial septal defect, ventricular septal defect, patent ductus arteriosus, and atrioventricular canal Obstruction to blood flow from ventricle= coarctation of aorta, aortic stenosis, pulmonic stenosis |
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Describe and list cyanotic heart defects:
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Conditions that result in: Decreased pulmonary blood flow= tetralogy of fallot, tricuspid stenosis Mixed (?) blood flow= transposition of great arteries total anomalous pulmonary venous connection trunchus arteriosus hypoplastic left heart syndrome |
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Describe an "acyanotic heart defect"
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-normally, blood flows from right to left -if defect such as hole in septum, then blood shifts from left to right through hole -called a left to right shunt because blood goes back to the lung -there is no mixing of oxygenated and deoxygenated blood GOING OUT TO SYSTEMIC CIRCULATION |
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Describe a "cyanotic heart defect"
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-if for some reason obstruction of the blood from the right side of the heart (ex: pulmonary hypertension or narrowing of the pulmonary valve) then increased pressure in the right ventricle of the heart causes a shift of blood from right to left -deoxygenated blood enters the systemic circulation |
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What blood flow patterns can alter the hemodynamic characteristics? |
-increased pulmonary blood flow -decreased pulmonary blood flow -obstruction to blood flow -mixed blood flow |
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What should you know about acyanotic defects?
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Defects allow blood to flow from left to right leading to increased pulmonary blood flow that eventually leads to congestive heart failure -atrial septal defect -ventricular septal defect -atrioventricular canal defect -patent ductus arteriosus |
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Describe obstructive defects:
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Impedes blood flow out of ventricles leading to CHF Right= cyanosis -coarctation of the aorta -aortic stenosis -pulmonic stenosis |
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Describe cyanotic defects
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-defects with decreased pulmonary blood flow lead to cyanosis -tetralogy of fallot -tricuspid atresia |
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Describe mixed defects:
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Saturated and desaturated blood mix within the heart or great arteries -signs and symptoms depend on the amount of mixing and amount of pulmonary blood flow -hypoxemia and CHF usually occur together -transposition of the great arteries -total anomalous pulmonary venous connection -truncus arteriosus -hypoplastic left heart syndrome |
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Describe diagnostic procedures for heart defects:
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-history -physical exam -cardiac catheterization |
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What are prenatal risk factors for heart defects?
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-maternal rubella during pregnancy -maternal alcoholism -maternal age over 40 years -maternal type 1 diabetes |
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What are genetic risk factors for heart defects?
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-sibling with congenital heart defect -parent with CHD -chromosomal aberrations such as Down's -born with other noncardiac congenital anomalies |
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Describe patent ductus arteriosus:
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Acyanotic heart defect Failure of the fetal ductus arteriosus to completely close after birth: it is the open vessel between the aorta and the pulmonary artery -may hear murmur -blood flows from the aorta (area of higher pressure) into the pulmonary artery (vessel with lower pressure) -thus more blood return to the lungs= increased pulmonary vascular congestion= increased workload on left side of heart (increased return of blood to left side of heart leads to increased stroke volume, causing increased aortic pressure mid to upper left sternal area) |
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What are signs and symptoms of patent ductus arteriosus? |
murmur as turbulent blood moves through the ductus arteriosus; tachycardia; widened pulse pressure; cardiomegaly; and bounding pulse. Respiratory symptoms.
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What is treatment for patent ductus arteriosus?
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May close on its own during first few weeks of life or may treat with indomethacin or need surgical ligation of patent vessel
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Describe coarctation of aorta:
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Localized narrowing of the aorta. Hemodynamics: increased pressure before defect, decreased pressure after defect. -resistance to blood flow out of left ventricle leads to decreased cardiac output -causes ventricular hypertrophy (like pumping iron) -leads t pulmonary vascular congestion |
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What are signs and symptoms of coarctation of aorta?
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-increased blood pressure and bounding pulses in areas receiving blood from vessels proximal to defect -weakened or absent femoral pulses -lower extremities cooler than upper because little blood gets through narrowing to the trunk and legs -muscle cramps due to anorexia -dizziness, headaches, faintaing, epistaxis -complications of intracranial hemorrhage and stroke, hypertension, CHF, all due to increased pressure in the upper body |
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What is the treatment for coarctation of aorta?
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Surgical resection of coerced portion with an end-to-end anastomosis or graft replacement (then hose-like material) of the constriction
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Describe atrial septal defect:
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Left to right shunt; acyanotic -pressure in the left atria causes left to right shift, increasing flow of oxygenated blood into right side of heart leading to increasing congestion in the lungs |
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What are signs and symptoms of atrial septal defect?
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-murmur -dyspnea due to increased blood return to lungs -fatigue -respiratory distress -activity intolerance -congestion -frequent respiratory infections |
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What is treatment for atrial septal defect?
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-surgical repair via open heart surgery -dacron material "thin felt" used to patch hole -optimum age is 5 years |
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Describe ventricular septal defect:
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-Left to right shift; acyanotic -abnormal open hole in septum between ventricles can range from being the size of a pinhole to absence of ventricular septum -pressure within the left ventricle causes blood flow toward defect to right ventricle, therefore increasing pulmonary vascular resistance -leads to same type of problems (respiratory) as ASD |
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What is treatment for ventricular septal defect?
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-surgical open heart required -may use purse stitch approach -if large defect then may use knitted dacron patch -banding of pulmonary artery may be used as a palliative measure |
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Describe pulmonary stenosis:
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-no shift of blood -narrowing at the entrance to the pulmonary artery -watch for right sided heart failure |
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Describe aortic stenosis:
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-resistance to flow out of left ventricle -decrease in cardiac output -leads to pulmonary vascular congestion -watch for left sided heart failure |
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Describe Tetralogy of Fallot:
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Only CYANOTIC defect you need to know about -most common cyanotic defect in children -causes right to left shift of blood -consists of four distinct defects: +ventricular septal defect (increased pressure in right ventricle forces unoxygenated blood through septal defect into left ventricle) +pulmonic stenosis (impedes flow of blood to the lungs) +over-riding aorta (directly receives blood from the right and left ventricles) +right ventricular hypertrophy (due to increased workload) |
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Describe the hemodynamics of tetralogy of fallot:
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-Pulmonic stenosis impedes flow of blood to the lungs -increased pressure in the right ventricle forces unoxygenated blood through septal defect to left ventricle -increased workload on the right ventricle causes hypertrophy -overriding aorta directly receives blood from the right and left ventricles |
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Describe the four abnormalities that result in insufficiently oxygenated blood being pumped through the body in tetralogy of fallot:
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1. Narrowing of the pulmonary valve 2. Thickening of the wall of the right ventricle 3. Displacement of aorta over ventricular septal defect 4. Ventricular septal defect: opening between the left and right ventricles |
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What are the signs and symptoms of tetralogy of Fallot?
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-Infants: cyanotic/hypoxic spells (blue spells), crying after feeding, child's needs exceed blood amount supplied, knee chest position -Children: physical evidence of cyanosis -clubbing of fingers -squatting to relieve chronic hypoxia -murmur, fainting, mental slowness due to chronic hypoxia to brain, seizures after exertion -low oxygen levels in the blood cause the lips, fingers, and toes to look blue (cyanotic) -often exhibit bluish skin during episodes of crying or feeding |
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Describe treatment for the hypercyanotic spells that occur in tetralogy of falot:
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-blue or tet spells Treatment= -place infant in knee-chest position -O2 100% mask -morphine IV -IV fluid replacement and volume expansion PRN |
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What is the treatment for tetralogy of fallot?
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-palliative surgical treatment aimed at relieving symptoms -create an artificial opening between aorta and pulmonary artery to increase pulmonary blood flow -Blalock-Taussing: subclavian artery-pulmonary artery anastomosis in older children (more blood returns to lungs for oxygenation) -Waterson-Cooley shunt: ascending aorta to right pulmonary artery Corrective treatment: -complete repair of defects -closure of VSD -pulmonic valvotomy -correction of overriding aorta |
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Describe transposition of great vessels:
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Cyanotic heart defect! -pulmonary artery and aorta are in reverse positions, pulmonary artery off left ventricle, aorta exits right ventricle -2 separate circulations -no communication between systemic and pulmonary circulations -sometimes other defects also exist |
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What are signs and symptoms of transposition of great vessels:
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-depends on type and size of associated defects -without link between systems-severely cyanotic and depressed at birth -large septal defect or patent ductus arteriosus may be less cyanotic but have signs and symptoms of CHF |
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What is treatment for transposition of great vessels?
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-surgical: palliative: prevent CHD -Surgery creates ASD (Blalock-Hanlen) -enlarge of existing ASD during catheterization (Rashkind) -pulmonary artery banding to decrease blood flow to lungs -create ductus arteriosus if pulmonic stenosis is present -complete repair: Mustard's operation is removal of atrial septum and creating new atrial septum for effective oxygenation |
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What are nursing goals for cyanotic defects?
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Prevent congenital heart disease by: -encourage rubella immunization in women because exposure during pregnancy puts them at high risk for having child with congenital heart defect -encourage early prenatal care, conscious dies, avoidance of drugs Assist diagnosis by: -good assessment: history of poor weight gain, poor feeding habits, pause during eating, exercise intolerance, unusual posturing, squatting, frequent respiratory tract infections -general assessment: color, pulse, respirations, blood pressure, examine chest, auscultate chest, vital signs, edema, chest pain Improve efficiency of heart by: -digoxin to decrease pulse rate and increase force of contraction. Check apical pulse for full minute before giving it. Withhold medication and call physician if infant pulse less than 90-110, older child less than 70-85. Nausea and vomiting indicate toxicity Reduce cardiac demands by: -adjusting activity to condition and capabilities, minimize crying, rest, avoid extremes of temperature Maintain nutrition: -no added salt, discourage foods with high salt contents which increase retention of fluids and thus increase work of the heart. Encourage well balanced diet, small frequent meals high in protein and calories. Main |
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Describe how the body attempts to compensate for decreased arterial O2 saturation by: |
-increasing pumping action of heart -increased force= results in cardiomegaly (pumping iron) -polycythemia -posturing |
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Describe the polycythemia that results from cyanotic defects:
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Body's response to decreased O2 supply. -increased production of erythrocytes to carry O2 to tissues -increased viscosity of blood due to added RBCs -results in sluggish circulation, oxygenated blood can not reach peripheral circulation especially capillaries (may be the cause of clubbing of the fingers) |
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Describe the posturing that results from cyanotic defects:
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Automatically learned. Infancy: flaccid with extremities extended (due to tissue hypoxia because flexed requires huge O2 supply). Flaccidity usually sign of progressive heart failure. Also, side lying position with knees bent toward chest, for same reason. Older child: squatting, which decreases venous return by occluding femoral veins through hip flexion to lessen workload on right side of heart and increase O2 saturation especially to vital organs |
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Describe the physical consequences that results from the compensatory mechanisms for cyanotic heart defects:
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-Growth retardation and exercise intolerance is direct consequence of inadequate nutrient intake and inadequate O2 for cell metabolism -failure to gain weight and decreased activity lead to poor muscle development. Activity self-limiting with severity of heart defect. -Recurrent respiratory infections due to pulmonary vascular congestion; susceptible to bacterial growth. |
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List some miscellaneous signs and symptoms of cyanotic heart defects: |
-dyspnea/tachypnea: lungs try to compensate for decreased O2 levels tachypnea= lung congestion tachycardia= heart attempts to increase cardiac output Cyanosis- due to deoxygenated hemoglobin. Located at blood vessels near the skin. -clubbing of fingers: due to persistent hypoxia-exact cause unknown. Thickening and flattening of distal phalanges of fingers. Characteristic finding of cyanotic heart conditions. Nails and fingers greater than 160 degree angle. -murmur: abnormal sound produced by vibrations with heart chambers or vessels |
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Blood backs up into right atrium and systemic circulation. Caused by left sided heart failure, cor pulmonale, right ventricular disease. Signs and symptoms include peripheral edema, ascites, fatigue, weight gain, increased heart rate, heart murmurs.
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Right sided heart failure
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