heart failure 2024.ppt , definition , causes , pathology , treatment

heart failure

1. Common cardio-vascular disorder Heart failure Prepared by : Mariam Adel

2. Under supervision of: Prof.Dr.Warda Yousef Mohamed professor of critical care and emergency nursing ,faculty of nursing, Cairo university Prof.Dr.Yousria Abd El Salam Assistant professor of critical care and emergency nursing ,faculty of nursing, Cairo university

3. Objectives Based on the content in this lecture, the reader should be able to: 1. Define heart failure. 2. Describe the classification systems used to define heart failure. 3. Explain the physiologic basis for the clinical manifestations of heart failure. 4. Describe expected clinical assessment findings for patients with heart failure .

4. Objectives, cont., 5 . Explain the standard pharmacologic therapies for chronic heart failure and acute exacerbation of chronic heart failure, and their rationale. 6. Describe the nonpharmacologic therapies for management of heart failure. 7. Define expected outcomes for therapeutic management of patients with heart failure. 8. Formulate a teaching plan for patients and families regarding heart failure.

5. Outlines 1-Define heart failure 2-Classification of heart failure 3-Pathophysiology of heart failure 4-Clinical manifestations of heart failure 5-Risk factor of heart failure 6-Medical and nursing management of heart failure 7- Recent researches about heart failure in nursing

6. Glossary Compensatory Mechanism :  An action taken by the body to continue physiological function despite an alteration in natural function . Cardiac  remodeling:  is a term that refers to changes in the heart’s size and shape that occur in response to cardiac disease or cardiac damage.When doctors talk about “ remodelling ,” they are usually talking about the left ventricle. Ventricular reserve: is the term used to describe the extent of increase or change in ventricular function that occurs during exercise or pharmacological stress.

7. Introduction Heart failure (HF) is a growing worldwide epidemic that results in significant morbidity and mortality in the aging population. HF is an important contributor to both the burden and cost of national healthcare expenditures, Heart failure is an epidemic disease which affects about 1% to 2% of the population worldwide . Schwinger, R. H. (2021).

8. Heart Failure definition Heart failure (HF) is a broad term referring to the inability of the heart to eject an adequate cardiac output to meet the oxygen and metabolic requirements of the body. A number of underlying disease processes may contribute to this " weak pump" syndrome, with coronary atherosclerosis, valvular heart disease, hypertension, and cardiomyopathy as the most common causes. Savarese , G., 2022

9. Pathophysiology and Pathogenesis cardiac output is determined by 2 factors: Heart Rate Stroke Volume Heart rate is the number of times the heart beats in a minute, and stroke volume is the volume of blood pumped out of the left ventricle with each cardiac contraction.  Schwinger , R. H. (2021).

10. Pathophysiology and Pathogenesis,cont., Three factors determine the stroke volume in a normal heart. They are: Preload = The amount of ventricular stretch prior to cardiac contraction determined by the pressure and volume of blood in the ventricle at the end of diastole. Afterload = The pressure and volume of blood in the ventricle during systole; The amount of resistance or the pressure against which the heart must overcome to pump blood during systole.   Myocardial Contractility = The inherent ability of the myocardial cells to contract and denotes the pumping capacity of the heart muscle . Roger , V. L. (2021).

11. Arrigo, M., Jessup, M., Mullens , W., Reza, N., Shah, A. M., Sliwa , K., & Mebazaa , A. (2020). Acute heart failure.  Nature Reviews Disease Primers ,  6 (1), 16.‏

12. Ventricular dysfunction can negatively affect the stroke volume. Ventricular dysfunction can be due to two reasons: Impaired Systolic Contraction (Systolic Dysfunction) = The ventricles, particularly the left ventricle, are unable to contract well during systole. Due to myocardial disease or damage as occurs in myocardial infarction and cardiomyopathies. Impaired Diastolic Relaxation (Diastolic Dysfunction) = The ventricles do not relax properly during diastole. Due to abnormal relaxation or stiffness of the myocardium as occurs in ventricular hypertrophy or restrictive cardiomyopathies.  Roger , V. L. (2021).

13. Pathophysiology Although HF refers to any cardiac insufficiency, left ventricular systolic dysfunction is the most common disorder. The pathophysiology of HF is a three-stage process, beginning with an initial insult to the myocardium (phase I), followed by a response phase (phase II), and resulting in the clinical syndrome known as HF, characterized by exhaustion of compensatory mechanisms (phase III). Park , J. J. (2021).

14. Phase I Phase I of HF is characterized by an initiating event ( eg , MI, viral infection, valvular heart disease, hypertension, idiopathic cardiomyopathy), which causes loss of myocytes . This cell loss or permanent damage to the myocytes can be either localized or diffuse , resulting in compromised ventricular function . • Result of phase I: Decreased cardiac output secondary to an initial insult to the myocardium . Park , J. J. (2021).

15. Phase II A number of adaptive mechanisms occur in response to the initial insult in an effort to maintain adequate cardiac output to meet the body's needs. This phase is sometimes referred to as the compensatory phase. These compensatory mechanisms or responses include the Frank-Starling response, myocardial remodeling, and the neuro-hormonal response . Park, J. J. (2021).

16. FRANK-STARLING RESPONCE As cardiac output decreases and the sympathetic nervous system is activated, alpha-1 receptors are stimulated , resulting in arteriolar and venous vasoconstriction. This adaptive response initially results in increased venous return to the ventricle, increased ventricular end-diastolic volume, stretching of the ventricular myocytes, and improved stroke volume. Park , J. J. (2021).

17. FRANK-STARLING RESPONSE, cont., Later , as overstretching of the ventricle occurs, this compensatory mechanism is lost, resulting in left ventricular decompensation and myocardial hypertrophy . Additionally , there is increased expression of granules in the left ventricle causing an increased release of brain natriuretic peptide (BNP). Increased BNP levels in the serum are used as markers of severity of ventricular failure . Park , J. J. (2021).

18. MYOCRDIAL HYPETROPHY (REMODELING) In response to increased vascular volume and decreased myocardial function (loss of the Frank-Starling response), the left ventricle dilates and hypertrophies. This distortion of the normal left ventricular anatomy causes mitral regurgitation and further left ventricular dilatation . Activation of angiotensin II, a by-product of the renin-angiotensin-aldosterone system (RAAS), systemically and in the endothelial cells of blood vessels, directly induces myocyte hypertrophy as well. Park , J. J. (2021).

19. MYOCRDIAL HYPETROPHY (REMODELING ) The result of these factors is decreased left ventricular reserve (stretch), increased preload (high residual volume in the ventricle following systole), and further mitral regurgitation . Park , J. J. (2021).

20. NEUROHORMONAL RESPONSE In response to decreased stroke volume/cardiac output and decreased renal perfusion, several neuro-hormonal systems are activated to compensate for the decrease in cardiac output, These include: 1. Adrenergic nervous system: Adrenergic nervous system activity is heightened in the setting of impaired ventricular function as a direct result of baroreceptor stimulation. These baroreceptors mediate the sympathetic nervous system, which in turn stimulates the beta-1 receptors . This results in an increase in heart rate and contractility . Park , J. J. (2021).

21. NEUROHORMONAL RESPONSE 2 . Renin-angiotensin-aldosterone system: Decreased renal perfusion stimulates the release of renin, increasing the production of angiotensin I and 11, and the release of aldosterone. This causes arteriolar vasoconstriction, decreased cardiac output, increased arterial BP and peripheral resistance, increased ventricular filling pressures, sodium and potassium retention (imbalance), increased volume overload, increased left ventricular wall stress, increased ventricular dilation and hypertrophy, and increased sympathetic nervous system arousal . Park , J. J. (2021).

22. NEUROHORMONAL RESPONSE 3 . Atrial natriuretic peptide (ANP): ANP is a counter regulatory hormone that opposes all three of the above systems, resulting in vasodilation and sodium excretion. ANP is produced in response to atrial distension and results in decreased formation of renin, decreased effects of angiotensin II, decreased release of aldosterone and vasopressin, and enhanced renal excretion of sodium and water. In chronic HF, the levels of ANP remain elevated, but are less so than in the acute phase (phase II ). Park , J. J. (2021).

23. Phase II The effects of the compensatory mechanisms in phase II lead to an increase in circulating volume and perfusion to vital organs. These mechanisms are self-limiting and a vicious cycle of increased afterload and volume overload results. The neuro-hormonal response is no longer beneficial in the chronic state but, as seen in phase III, becomes detrimental leading to changes in the myocyte DNA, resulting in programmed cell death (apoptosis) and further loss of myocytes . Park, J. J. (2021).

24. • Result of phase II; Ventricular hypertrophy weakened myocytes increased arteriolar resistance increased vascular volume increased ventricular wall stress occur in an effort to maintain adequate cardiac output.

25. Phase/II When the adaptive mechanisms of phase II fail, the clinical syndrome of HF follows. This third phase of HF is extremely variable in onset and presentation. The clinical expression and course of the disease is determined by the extent of the initial insult and myocyte damage, the severity of hemodynamic burden (volume overload), and the patient's individual neuro-hormonal response to these changes. Park , J. J. (2021).

26. Phase III is characterized by a progressive deterioration of cardiovascular functioning due to the relationship between compromised left ventricular function and excessive cardiac afterload . • Result of phase lll : Clinical sign and symptoms of HF are evident, resulting in decreased functional status and activity intolerance for the patient . Park , J. J. (2021).

27. Causes Heart failure is caused by several disorders, including diseases affecting the pericardium, myocardium, endocardium, cardiac valves, vasculature, or metabolism. The most common causes of systolic dysfunction ( HFrEF ) are idiopathic dilated cardiomyopathy (DCM), coronary heart disease (ischemic), hypertension, and valvular disease. Malik , ( 2023).

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29. Risk Factors Coronary artery disease Myocardial infarction Hypertension Diabetes Obesity Smoking Alcohol use disorder Atrial fibrillation Thyroid diseases Congenital heart disease Aortic stenosis Malik, (2023).

30. Assessment Symptoms of heart failure include those due to excess fluid accumulation (dyspnea, orthopnea, edema, pain from hepatic congestion, and abdominal distention from ascites) and those due to a reduction in cardiac output (fatigue, weakness) most pronounced with physical exertion . Malik , (2023).

31. Acute and subacute presentations (days to weeks) are characterized by shortness of breath at rest and/or with exertion, orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to acute hepatic congestion (right heart failure). Palpitations, with or without lightheadedness, can occur if patients develop atrial or ventricular tachyarrhythmias . Malik , (2023).

32. Chronic presentations (months) differ in that fatigue, anorexia, abdominal distension, and peripheral edema may be more pronounced than dyspnea. The anorexia is secondary to several factors, including poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion. Malik, (2023).

33. Characteristic features: Pulsus alternans phenomenon characterized by evenly spaced alternating strong and weak peripheral pulses. Apical impulse: Laterally displaced past the midclavicular line, usually indicative of left ventricular enlargement. S3 gallop: A low-frequency, brief vibration occurring in early diastole at the end of the rapid diastolic filling period of the right or left ventricle. It is the most sensitive indicator of ventricular dysfunction. Peripheral edema Pulmonary rale Malik, (2023).

34. Clinical presentation Regardless of the underlying cause of the weak pump, patients with HF present with clinical signs and symptoms of intravascular and interstitial volume overload, as well as manifestations of inadequate tissue perfusion. Common findings in HF include: • Dyspnea (especially with exertion, commonly severe in the acute setting) • Paroxysmal nocturnal dyspnea • Pulmonary edema (pronounced crackles) • Jugular venous distention (JVD) • Chest discomfort or tightness • Peripheral edema • Cool, pale. cyanotic skin • Oliguria • Reported weight gain • Fatigue Malik , (2023).

35. Classification Systems New York Heart Association Functional Classification Class I: No limitation of physical activity . Ordinary physical activity does not cause undue fatigue or dyspnea . Class II: Slight limitation of physical activity . Comfortable at rest, but ordinary physical activity results in fatigue or dyspnea . Malik , (2023).

36. New York Heart Association Functional Classification Class III: Comfortable at rest but minimal activity causes symptoms of heart failure including dyspnea or fatigue . Class IV: Unable to carry on any physical activity without symptoms. Symptoms are present even at rest. If any physical activity is undertaken, symptoms are increased . Malik, (2023).

37. American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines for Stages of Heart Failure A . Patients at high risk for heart failure because of the presence of conditions that are strongly associated with the development of heart failure. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of heart failure. Malik , (2023).

38. B. Patients who have structural heart disease that is strongly associated with the development of heart failure but who have never shown signs or symptoms of heart failure. C . Patients who have current or prior symptoms of heart failure associated with underlying structural heart disease. D. Patients with advanced structural heart disease and marked symptoms of heart failure at rest despite maximal medical therapy and who require specialized interventions. Malik , (2023).

39. Classifications of Heart Failure Heart failure can be classified based on which side of the heart is predominantly affected: Left Heart Failure – The left ventricular output decreases and the left atrial and pulmonary venous pressure increase as in: Myocardial infarction Aortic valve disease Mitral stenosis Right Heat Failure – The right ventricular output is reduced, and the right atrial and systemic venous pressure increase as in: Pulmonary stenosis Pulmonary hypertension Pulmonary embolism Biventricular Heart Failure – The left and right ventricles are affected and fail as in: Cardiomyopathies When right ventricular failure follows left ventricular failure due to development of pulmonary hypertension.  Schwinger , R. H. (2021).

40. Classifications of Heart Failure Heart failure can also be classified as acute and chronic : Acute Heart Failure – Indicates an acute left ventricular dysfunction leading to acute pulmonary edema as occurs in: Acute myocardial infarction Severe hypertension Acute myocarditis Similarly, acute failure of the right ventricle occurs in acute pulmonary embolism Chronic Heart Failure – Occurs in all types of heart diseases and indicates: Recurrent attacks of heart failure and persistent symptoms Chronic heart failure is often referred as “Congestive Heart Failure”.  Schwinger , R. H. (2021).

41. Classifications of Heart Failure Another classification of heart failure is based on the ejection fraction which is calculated using echocardiography. Heart Failure with Reduced Ejection Fraction ( HFrEF ) – When the EF is below 40%. Heart Failure with Preserved Ejection Fraction ( HFpEF ) – When the EF is above 50%. Heart Failure with Mid-Range Ejection Fraction ( HFmrEF ) – Denotes the gray zone of ejection fractions between 40-50%.  The ejection fraction (EF) is the percentage of the End Diastolic Volume (EDV) that is ejected out of the ventricle with each ventricular contraction (systole). The EF is expressed as a percentage. Ejection Fraction = (Stroke Volume/End Diastolic Volume) x 100 The Stroke Volume (SV) is the difference between the End Diastolic Volume (EDV) and the End Systolic Volume (ESV ). Schwinger, R. H. (2021).

42. Evaluation Electrocardiogram (ECG): Important for identifying evidence of acute or prior myocardial infarction or acute ischemia, rhythm abnormalities, such as atrial fibrillation.  Chest x-ray: Characteristic findings are cardiac-to-thoracic width ratio above 50%, cephalization of the pulmonary vessels, Kerley B-lines, and pleural effusions. Blood test: Cardiac troponin, complete blood count, serum electrolytes, blood urea nitrogen, creatinine, liver function test, and brain natriuretic peptide (BNP). BNP (or NT- proBNP ) level adds greater diagnostic value to the history and physical examination than other initial tests mentioned above. Transthoracic echocardiogram: To determine ventricular function and hemodynamics . Malik , (2023).

43. Congestive Heart Failure: Chest x-ray of congestive heart failure showing cardiomegaly and pulmonary edema.

44. Principle of management of heart failure Goals of patient management in HF revolve around four general principles: (1 ) treatment of the underlying cause { eg , ischemia, valvular dysfunction). (2) management of fluid volume overload. (3) improvement of ventricular function. (4) patient and family education.

45. limiting the Initial Insult and treating the underlying cause The most effective, but often the most difficult, management strategy for HF is to limit the damage done by the initial insult. This limitation of myocardial damage and cell loss maximizes the amount of viable ventricular muscle, myocardial contractility, and overall ventricular function. • Patient with AMI receives immediate treatment either with fibrinolytic therapy if eligible or transfer to the cardiac catheterization laboratory for primary PCI. • Patients with persistent ischemia may benefit from revascularization as a preventive measure against eventual tissue necrosis. • Valve replacement or repair or other surgical corrections (ventricular reconstruction surgery) is undertaken as soon as possible to prevent prolonged overstretching of the ventricular myocardium . Schwinger , R. H. (2021).

46. Management of fluid Volume Overload Decrease preload by administering diuretic therapy, limiting dietary sodium, and restricting free water . • Diuretics are initiated according to the severity of the patient's signs and symptoms. Thiazide diuretics may be added later if the patient does not respond to the loop diuretics. • Sodium and fluid intake are monitored carefully, with sodium not exceeding 2 g/day and free water not exceeding 1500 ml in a 24-hour period. • Serum sodium and potassium are monitored on a regular basis to prevent inadvertent electrolyte imbalances. • Use daily weights to evaluate for changes in fluid status . Schwinger , R. H. (2021).

47. Improvement of Left Ventricular Function Improvement in left ventricular function is accomplished by decreasing the workload on the heart with preload and afterload reduction and by augmenting ventricular contractility . Ventricular function is often measured in the acute setting by monitoring Cl or CO directly. • Decrease preload. • Decrease afterload by administration of pharmacologic therapy, including ACE inhibitors and vasodilators . Schwinger , R. H. (2021).

48. ACE inhibitors are recommended in all HF patients with a left ventricular EF less than 40% unless otherwise contraindicated. Contraindications to ACE inhibitor therapy include previous intolerance, potassium greater than 5.5 mEq /L, hypotension with systolic BP less than 90 mm Hg, and serum creatinine greater than 3 . 0 mg/ dL . Vasodilators may also be used in conjunction with diuretics and ACE inhibitors if fur ther afterload reduction is necessary. Schwinger , R. H. (2021).

49. Nitrates are often used concomitantly with ACE inhibitors and diuretics to augment afterload reduction, especially in the case of underlying atherosclerotic disease, the largest single contributor to HF. Angiotensin receptor blockers (ARBs) may be used if the patient does not tolerate the side effects of an ACE inhibitor ( eg , cough ). Schwinger , R. H. (2021).

50. ACE inhibitors and beta-blockers are considered cornerstone therapy for HF in an effort to reverse the remodeling of the left ventricle . Aldosterone antagonists may be used as add-on therapy. Isosorbide dinitrate and hydralazine may be effective , particularly in black patients . Digoxin has been shown to improve symptoms but is no longer considered to be first-line therapy unless paroxysmal atrial fibrillation or atrial flutter is present. Digoxin may be used to control the ventricular rate in this situation . Schwinger, R. H. (2021).

51. • A newer class of medications called angiotensin receptor neprilysin inhibitors ( ARNis ) are used in the management of heart failure with reduced ejection fraction. V alsartan ( Entresto ) is an example of this class of medications. It contains an ARB and a neprilysin inhibitor. The neprilysin inhibitor improves renal blood flow and promotes the loss of sodium . The ARB lowers blood pressure and reduces myocardial workload. Schwinger , R. H. (2021).

52. Beta-blockers are also used to reduce the incidence of ventricular tachycardia (VT) and ventricular fibrillation, the most common cause of death in HF patients. Recommended beta-blockers for the management of HF include carvedilol, metoprolol, and bisoprolol . Caution is taken when initiating a beta-blocker in a patient with reactive airway disease . Schwinger , R. H. (2021).

53. • Dual-chamber biventricular pacemaker/implantable cardioverter defibrillator (ICD ): There have been several studies demonstrating significantly improved outcomes (quality of life, survival rates, etc ) with the use of a dual-chamber biventricular pacemaker . This technology stimulates both ventricles simultaneously, causing both to contract at the same time resulting in a narrowing of the QRS complex and improved myocardial contractility and cardiac output. Often the pacing technology is combined with an ICD because sudden cardiac death related to VT/fibrillation is the most common cause of death in these patients . Schwinger , R. H. (2021).

54. Cardiac assist devices (left ventricular, right ventricular, or both) can provide temporary maintenance or preservation of ventricular function, especially as a bridge to recovery, bridge to cardiac transplantation, or as destination therapy (discharge to home). These devices may be inserted percutaneously via the femoral artery or femoral vein, or surgically using the medial sternotomy or thoracotomy approach . Schwinger , R. H. (2021).

55. Intra-aortic balloon pump (IABP) : Femoral or bra chia! artery cannulation with the IABP allows for ventricular support , but restricts the patient to bed rest (femoral primarily) and compromises arterial flow to the cannulated limb . Schwinger , R. H. (2021).

56. Patient Education Patients who present with HF to the critical care unit have high acuity levels, require more intensive interventions , and have an increased need for emotional support surrounding the serious nature of the hospital admission. Patient education, which is appropriately addressed in the acute care setting, includes the following: • Both patient and family may require crisis interventions. The nurse may help by encouraging the verbalization of fears related to role adaptations or changes in family responsibility, lifestyle alterations and limitations, and death and dying.

57. Patient Education, cont., • Family involvement in the critical care phase is strongly encouraged, including assistance with activities of daily living such as bathing, and "'patterning" of daily activities to allow for frequent periods of rest and spacing of exertional activity. In addition, family involvement in reading or other leisure activity with the patient is often restful and relaxing, and may be useful as a diversional activity. If possible, the family is also present for reinforcement of patient teaching regarding the medical regimen, the importance of fluid and sodium restriction , and the need for daily weights .

58. Patient Education, cont., Helping patients control both their heart failure and their comorbid diseases empowers them and gives them a sense of control that also helps to limit hospitalization. Disease management is an option for patients with multiple comorbidities who find self-care in heart failure to be particularly challenging. There is some evidence that disease management improves quality of life, decreases hospitalizations, and decreases cost of care for patients with heart failure.

59. Patient Education, cont., Home care provides many opportunities for disease management. Discharge planning begins with the first day of hospitalization. A program of education, referral, and follow-up is initiated with the goal of preventing further hospitalization. Carefully planned transitions from hospital to home are linked to decreased hospitalizations for those with heart failure. However , patients must collaborate with health care providers to maximize this Benefit .

60. Nursing Management objectives: The nursing care plan for patients with HF should include : Relieving fluid overload symptoms Relieving symptoms of anxiety and fatigue Promoting physical activity Increasing medication compliance Decreasing adverse effects of treatment Teaching patients about dietary restrictions Teaching patient about self-monitoring of symptoms Teaching patients about daily weight monitoring

61. Teaching Guide Living With Heart Failure Medications • Take all medications as instructed. If you cannot afford them , please let your provider know so that you can be put in touch with someone to help . • Do not stop taking medication because you feel better. These are lifetime medications in most instances. Some of the medications will need to be adjusted over time, but your health care provider will discuss the changes with you . • Take your medications about the same time every day.

62. Medications • You may be taking several drugs. These medications do not interfere with each other, and they are given together so that they can work together to do more than any one or two of them can do alone. • Do not let your medication supply run out because stopping some medications suddenly can cause serious problems . • If you are going out for a few hours and will not have easy access to a bathroom when you need it, hold off on your diuretic until you return home. Do not skip a day’s dose of diuretic because this could lead to serious water accumulations and worsening of your heart failure.

63. Diet • Restrict your salt intake by removing the salt shaker from the table and the food preparation area. Do not add salt to any food you are cooking or any food on your plate. • Avoid foods that have a high salt content naturally or because of the way they are preserved. Foods such as canned soup, canned vegetables, canned meats, foods frozen in sauces, Avoid fast food such as hamburgers, French fries, fried chicken, and tacos. • Seasonings such as pepper, Mrs. Dash, onion and garlic powder, herbs, seeds, and spices are acceptable. • Fresh or frozen vegetables (frozen without sauces), fresh lean meats and poultry, and fish (not fried) are all good choices.

64. Daily Weights • Weigh yourself every day at about the same time and record the value. • The best time to weigh yourself is in the morning when you first get up and after you go to the bathroom. • Weigh yourself without clothes if possible. • Record your weight and the date in a daily diary. Bring this diary with you to the office when you visit your health care provider. • Call if your weight goes up more than 2 pounds overnight and does not go back to baseline the next day, or if you gain more than 3 pounds in a week.

65. Activity • Stay as active as possible. • The stronger your skeletal muscles are, the easier it is for your heart. • Do not use heart rate as a measure of adequacy of exercise effort. • If you get tired or short of breath, stop and rest, and then try again. The goal is 15 to 20 minutes of continuous activity each day. • There are no speed or distance goals, and walking at whatever pace you can accomplish is a good choice. Homemaking and gardening are good choices as well. Choose an activity that you enjoy .

66. Activity • Shortness of breath is uncomfortable but not dangerous. It is an indication that you are nearing the end of your exercise tolerance for this period, but once your breathing normalizes, you can go again. If you stop before you get short of breath out of fear, you will not be able to increase your activity tolerance. • If you have any questions about how much exercise you can tolerate, discuss it with your health care provider. That person is the best advisor for you because you are well known to him. • Do not lift weights unless your health care provider has specifically said it is an acceptable activity for you.

67. Call Your Health Care Provider If • Your weight increases or decreases suddenly. • You begin waking up at night short of breath and need to sit up to breathe. • You start needing more pillows at night to breathe when you lie down, or you are unable to lie down. • You become short of breath at rest. • You cannot walk up stairs that you used to climb regularly because now it makes you too short of breath or tired. • Your feet and legs start to swell. • You faint or feel as though you are going to faint .

68. Complications of Heart Failure The following complications may occur in congestive heart failure: Renal Failure . Poor renal perfusion caused by the low cardiac output in CHF leads to renal failure. Liver Dysfunction . Poor hepatic perfusion and congestion secondary to raised systemic venous pressure may lead to mild jaundice and liver dysfunction. Electrolyte Disturbances . Hypokalemia may follow the use of loop diuretics. Hyponatremia is a complication which follows use of diuretics which flush out salt and water from the body.

69. 4.Atrial and Ventricular Arrhythmias . Many different types of tachy -arrhythmias can occur in CHF. But the most common is atrial fibrillation which can cause harm to the patient, as it can lead to thromboembolism and is a common cause of stroke in heart failure.  5.Thromboembolism . Prolonged bed rest and venous pooling in the lower limbs can lead to deep vein thrombosis (DVT) and pulmonary embolism (PE). 6.Sudden Cardiac Death is not an uncommon complication and is seen in almost half of the patients with CHF. Ventricular fibrillation is usually the terminal event.  7.Infections . Recurrent respiratory infections especially pneumonia are a frequent complication of CHF. When valvular lesions are present, the risk of infective endocarditis is high and may lead to resistant heart failure and death. 8.Cardiac Cachexia . This denotes extreme weight loss with fatigue which may occur in CCF due to muscle wasting.

70. Recent research about heart failure in nursing Influence of Comprehensive Nursing Care on Heart Failure Patient Management: A Systematic Review and Meta-Analysis     Conclusion: Comprehensive nursing care improves clinical outcomes and quality of life for heart failure patients. This study stresses the need to add comprehensive nurse interventions in normal heart failure treatment programmes .

71. Nursing care of the patient hospitalized with heart failure: A scientific statement from the American Association of Heart Failure Nurses Conclusion Nurses play a pivotal role in the healthcare team, providing essential care of patients with HF. Their contributions encompass various roles such as skilled clinician, problem-solvers, educators, patient advocates, care coordinators, and liaisons between healthcare teams. nurses influence HF care across the entire spectrum including prevention, phases of  early diagnosis  and acute decompensation, recovery, and end-stage disease . Nurses are in a unique position to address HF care comprehensively and holistically, considering all aspects of the condition for patients and their caregivers.

72. Effectiveness of Heart Failure Nursing Protocol (HF-NP) on quality of life of patients with heart failure     CONCLUSION :  HF-NP was effective in improving HF outcomes. It can be used to train patients and their family members regarding the debilitating illness, after doing a large study, and it can be incorporated into the health policy later.

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