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64 Cards in this Set
- Front
- Back
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What does the long-term survival of clients with heart disease depend on?
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Client compliance with therapy and a coordinated interdisciplinary approach to ensure the best management of the illness and the highest possible quality of life
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What is heart failure?
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1. A general term for the inadequacy of the heart to pump blood throughout the body
2. This deficit causes insufficient perfusion of body tissues with vital nutrients and oxygen |
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Where do most heart failure begin?
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With failure of the left ventricle and progresses to failure of both ventricles
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What causes left-sided heart (ventricular) failure?
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1. Hypertensive, coronary artery, and valvular disease involving the mitral or aortic valve
2. Decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in the pulmonary vessels indicate left ventricular failure |
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What are the two subtypes of left-sided heart failure (CHF)?
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Systolic and diastolic heart failure
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What is systolic heart failure?
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Systolic ventricular dysfunction that results when the heart is unable to contract forcefully enough during systole to eject adequate amounts of blood into the circulation
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What are the manifestations of systolic dysfunction?
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Symptoms of inadequate tissue perfusion or pulmonary and systemic congestion
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What is diastolic heart failure?
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Diastolic ventricular function that occurs when the left ventricle is unable to relax adequately during diastole
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What are the characteristics of diastolic heart failure?
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1. Inadequate relaxation or "stiffening" prevents the ventricle from filling with sufficient blood to ensure an adequate cardiac output
2. The ejection fraction may remain near normal |
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What are the symptoms of diastolic heart failure?
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Similar to those of systolic dysfunction = symptoms of inadequate tissue perfusion or pulmonary and systemic congestion
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What causes right-sided heart (ventricular) failure?
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1. Left ventricular failure
2. Right ventricular myocardial infarction 3. Pulmonary hypertension |
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What happens in right-sided heart (ventricular) failure?
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The right ventricle is unable to empty completely. Increased volume and pressure develop in the systemic veins, and systemic venous congestion develops with peripheral edema.
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What is high-output failure?
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When cardiac output remains normal or above normal, unlike left- and right-sided heart failure, which are typically low-output states
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What causes high-output heart failure?
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1. Increased metabolic needs
2. Hyperkinetic conditions, such as septicemia (fever), anemia, and hyperthyroidism |
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What is Stage A heart failure?
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A high risk for HF without any structural heart changes or disorders
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What is Stage B heart failure?
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A structural disorder but no development of any symptoms of the disease
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What is Stage C heart failure?
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A current or past history of HF with a structural disorder
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What is Stage D heart failure?
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1. End-stage disease
2. The client with stage D illness requires ongoing, chronic support and treatments, including possible hospice care or heart transplantation |
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What is Class I heart failure?
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1. Clients with cardiac disease but without resulting limitations of physical activity
2. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain |
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What is Class II heart failure?
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1. Clients with cardiac disease resulting in slight limitation of physical activity
2. They are comfortable at rest 3. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain |
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What is Class III heart failure?
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1. Clients with cardiac disease resulting in marked limitation of physical activity
2. They are comfortable at rest 3. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain |
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What is Class IV heart failure?
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1. Clients with cardiac disease resulting in inability to carry on any physical activity without discomfort
2. Symptoms of cardiac insufficiency or of the anginal syndrome may be present, even at rest 3. If any physical activity is undertaken, discomfort is increased |
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What happens when cardiac output is insufficient to meet the demands of the body?
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Compensatory mechanisms operate to improve cardiac output
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What are the compensatory mechanisms?
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1. Sympathetic nervous system stimulation
2. Renin-angiotensin system (RAS) activation 3. Other neurohumoral responses 4. Myocardial hypertrophy |
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What is the effect of the compensatory mechanisms over time?
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Although these mechanisms may initially increase cardiac output, they eventually have a damaging effect on pump function
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What is sympathetic nervous system stimulation?
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Increased release of catecholamines (epi & norepi) to increase heart rate and BP
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What are the effects of sympathetic nervous system stimulation?
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1. Initial increase in HR results in an immediate increase in cardiac output
2. Over time, if HR becomes too rapid, diastolic filling time is limited and CO may start to decline 3. An increase in HR also significantly increases oxygen demand by the myocardium. If the heart is poorly perfused because of arteriosclerosis, HF may worsen. 4. Stroke volume is also improved by sympathetic stimulation. Sympathetic stimulation increases venous return to the heart, which further stretches the myocardial fibers, causing dilation. Increased myocardial stretch results in more forceful contraction. More forceful contractions increase SV and CO. After a critical point is reached within the cardiac muscle, further volume and stretch will reduce the force of contraction and CO. 5. Sympathetic stimulation also results in arterial vasoconstriction. Constriction of the arteries has the benefit of maintaining blood pressure and improving tissue perfusion in low-output states; however, constriction of the arteries increases afterload, the resistance against which the heart must pump. Afterload is the major determinant of myocardial oxygen requirements. As afterload increases, the left ventricle requires more energy to eject its contents, and SV may decline. |
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What are the effects of the renin-angiotensin system activation?
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1. Reduced blood flow to the kidneys, a common occurrence in low-output states, results in activation of the renin-angiotensin system (RAS)
2. Vasoconstriction becomes more pronounced in response to angiotensin II, and aldosterone secretion causes sodium and water retention 3. Preload and afterload increase; angiotensin II contributes to ventricular remodeling, resulting in progressive myocyte (myocardial cell) contractile dysfunction over time |
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What are the other neurohumoral responses to heart failure?
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1. Heart muscle cell injury causes an immune response. Proinflammatory cytokines, such as tumor necrosis factor (TNF) and interleukins (IL-1 and IL-6) are released, especially with left-sided HF. These substances contribute to ventricular remodeling.
2. Natriuretic peptides are hormones that promote vasodilation and diuresis through sodium loss in the renal tubules. The B-type natriuretic peptide (BNP), produced and released by the ventricles, increases to counterbalance the RAS, thus decreasing preload. 3. Low CO causes decreased cerebral perfusion. As a result the posterior pituitary gland secretes vasopressin (antidiuretic hormone, or ADH). The hormone causes vasoconstriction and fluid retention, which worsen HF. 4. Endothelin is secreted by endothelial cells when they are stretched. As the myocardial fibers are stretched in clients with HF, this potent vasoconstrictor is released, which increases peripheral resistance and hypertension. HF worsens as a result of these actions. |
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What is the final compensatory mechanism to heart failure?
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Myocardial hypertrophy, with or without chamber dilation
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What are the effects of myocardial hypertrophy?
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1. The walls of the heart thicken to provide more muscle mass, which results in more forceful contractions, further increasing cardiac output
2. Cardiac muscle, however, may hypertrophy more rapidly than collateral circulation can provide adequate blood supply to the muscle 3. Often a hypertrophied heart is slightly oxygen deprived |
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What are the side effects of the compensatory mechanisms?
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All the compensatory mechanisms contribute to an increase in the consumption of myocardial oxygen. When the demand for oxygen increases and the myocardial reserve has been exhausted, clinical manifestations of HF develop.
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What are the common causes of heart failure?
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1. Hypertension (75%)
2. CAD 3. Cardiomyopathy 4. Substance abuse (alcohol/drugs) 5. Valvular defects 6. Congenital defects 7. Cardiac infections and inflammations 8. Hyperkinetic conditions |
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What are the causes of right-sided HF in the absence of left-sided HF?
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1. Chronic obstructive pulmonary disease (COPD)
2. Cystic fibrosis 3. Acute respiratory distress syndrome (ARDS) |
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What are the key features of left-sided heart failure?
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1. Decreased Cardiac Output
2. Fatigue 3. Weakness 4. Oliguria during the day 5. Angina 6. Confusion, restlessness 7. Dizziness 8. Tachycardia, palpitations 9. Pallor 10. Weak peripheral pulses 11. Cool extremities 12. Pulmonary Congestion 13. Hacking cough, worse at night 14. Dyspnea/breathlessness 15. Crackles or wheezes in lungs 16. Frothy, pink-tinged sputum 17. Tachypnea 18. S3/S4 summation gallop |
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What are the key features of right-sided heart failure?
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1. Systemic Congestion
2. Jugular vein distention 3. Enlarged liver and spleen 4. Anorexia and nausea 5. Dependent edema (legs and sacrum) 6. Distended abdomen 7. Swollen hands and fingers 8. Polyuria at night 9. Weight gain 10. Increased blood pressure (from excess volume) or decreased blood pressure (from failure) |
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What is an early clinical manifestation of left-sided heart failure?
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A cough that is irritating, nocturnal, and usually nonproductive
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What is a late clinical manifestation of left-sided heart failure?
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Frothy, pink-tinged sputum — a sign of pulmonary edema (indication of severe HF)
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What is paroxysmal nocturnal dyspnea (PND)?
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Feeling of breathlessness 2 to 5 hours after falling asleep related to left-sided heart failure
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What relieves paroxysmal nocturnal dyspnea (PND)?
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1. Sitting upright
2. Dangling the feet 3. Walking usually relieves this condition |
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How is proportional pulse pressure calculated?
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(SBP-DBP)/SBP
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What does the proportional pulse pressure indicate?
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A proportional pulse pressure less than 25% indicates severely compromised cardiac output
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What is the purpose of the B-type natriuretic peptide (BNP) lab test?
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Differentiates between the dyspnea of HF and that associated with lung dysfunction
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What lab assessment is considered for HF in older adults?
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Thyroxine (T4) and thyroid-stimulating hormone (TSH) levels should be determined in clients who are over 65 years of age, have atrial fibrillation, or have evidence of thyroid disease because HF may be caused or aggravated by hypothyroidism or hyperthyroidism
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What are the advantages of EKGs?
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May demonstrate ventricular hypertrophy, dysrhythmias, and any degree of myocardial ischemia, injury, or infarction
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What are the disadvantages of EKGs?
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It is not helpful in determining the presence or extent of HF
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What are the primary nursing diagnoses for clients with HF?
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1. Impaired Gas Exchange related to ventilation perfusion imbalance
2. Decreased Cardiac Output related to altered contractility, preload, and afterload 3. Activity Intolerance related to an imbalance between oxygen supply and demand |
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What is the primary collaborative problem of clients with HF?
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Potential for Pulmonary Edema
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What are the other collaborative problems of clients with HF?
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1. Excess Fluid Volume related to compromised regulatory mechanism
2. Acute Confusion related to delirium 3. Ineffective Therapeutic Regimen Management related to social support deficits, complexity of therapeutic regimen, or knowledge deficit 4. Anxiety related to stress, change in health status and role function, or threat of death 5. Ineffective Tissue Perfusion: Cerebral related to mechanical reduction of arterial blood flow 6. Impaired Physical Mobility related to limited cardiovascular endurance 7. Risk for Ineffective Tissue Perfusion: Renal related to hypovolemia 8. Potential for Pneumonia 9. Potential for Dysrhythmias |
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What are the commonly used drug classifications for clients with HF?
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1. Angiotensin-converting enzyme (ACE) inhibitors
2. Diuretics 3. Human B-type natriuretic peptides 4. Nitrates 5. Inotropics (i.e. Digitalis) 6. Beta-adrenergic blockers |
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What is the action of ACE inhibitors?
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Reduce the resistance to left ventricular ejection (afterload)
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What is the action of Human B-type natriuretic peptides?
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Reduce the resistance to left ventricular ejection (afterload)
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What is the action of diuretics?
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Enhance the renal excretion of sodium and water by reducing circulating blood volume, decreasing preload, and reducing systemic and pulmonary congestion
(Reduce fluid retention) |
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What is the action of nitrates?
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1. Venous vasodilator to return venous vasculature to a more normal capacity
2. Decreasing the volume of blood returning to the heart 3. Improving left ventricular function |
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What is the action of Digitalis?
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Increase cardiac contractility
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What is the action of beta-adrenergic blockers?
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Reverse the effects of sympathetic stimulation and catecholamines that worsen cardiac function
("fight-or-flight" overstimulation effects) |
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What are the nonsurgical therapy for clients with HF?
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1. Continuous positive airway pressure (CPAP)
2. Cardiac resynchronization therapy (CRT) 3. Investigative gene therapy |
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What are the benefits of continuous positive airway pressure (CPAP)?
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1. Improves sleep apnea
2. Improves cardiac output and ejection fraction by decreasing afterload and preload, blood pressure, and dysrhythmias |
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What is sleep apnea directly correlated with?
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Coronary artery disease as a result of diminished oxygen supply to the heart during apneic episodes
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What is the purpose of cardiac resynchronization therapy (CRT)?
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Provide electrical stimulation to induce more synchronous ventricular contractions to improve EF, CO, and mean arterial pressure
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What are the expected outcomes for activity intolerance in clients with HF?
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1. Balance activity and rest
2. Use naps to restore energy 3. Recognize energy limitations 4. Organize activities to conserve energy 5. Adapt lifestyle to energy level 6. Report adequate endurance for activity |
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What are the complications of pulmonary edema?
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1. Left ventricle fails to eject sufficient blood
2. Pressure increases in the lungs because of the accumulated blood. The increased pressure causes fluid to leak across the pulmonary capillaries and into the pulmonary interstitium. |
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What is the care for clients with pulmonary edema?
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1. Identify the client's chief complaint
2. If the client's blood pressure is adequate, place the client in a high Fowler's position 3. Auscultate the client's lungs (posterior assessment) 4. Ensure that vascular access is present, and check for patency 5. Provide oxygen as ordered 6. Provide an IV diuretic (usually furosemide) as prescribed 7. Anticipate urine output 5 to 15 minutes after diuretic administration; catheterize if ordered 8. Monitor blood pressure, respiratory rate, pulse oximetry, pulse, cardiac rhythm, and the client's subjective report of ability to breathe 9. Provide additional medications as prescribed (usually morphine sulfate or nitroglycerin) 10. Provide comfort measures and reassurance 11. Notify the health care provider if the client does not experience a rapid improvement and diuresis |
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What are the indicators of worsening HF?
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1. Rapid weight gain (3 pounds in a week or 1 to 2 pounds overnight)
2. Decrease in exercise tolerance lasting 2 to 3 days 3. Cold symptoms (cough) lasting more than 3 to 5 days 4. Excessive awakening at night to urinate 5. Development of dyspnea or angina at rest or worsening angina 6. Increased swelling in the feet, ankles, or hands |
