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  • The preload is often expressed as the end-diastolic pressure/ volume of the left ventricle and is clinically assessed by measuring the right atrial pressure. However, the preload is not only dependent on intravascular volume; it is also influenced by any restriction to ventricular filling.
  • To eject blood, the ventricle must overcome the resistance cause by tension in the aorta and systemic vessels.The final determinant of stroke volume is afterload. In basic terms, afterload is the load that the pump has to work against, which is usually clinically estimated by the mean arterial pressure. The normal cardiac output is relatively insensitive to afterload up to 140 mm Hg. However, the afterload represents not only the vascular resistance but also the wall tension and intrathoracic pressure that the myocardium must work against. Together, these 3 variables are impaired in the patient with CHF.
  • The second variable of stroke volume is cardiac contractility, which represents the muscular pumping of the heart and is commonly expressed as the ejection fraction. Based on autonomic input, the heart will respond to the same preload with different stroke volumes, depending on inherent characteristics of the heart. A heart with normal systolic function will maintain an ejection fraction of over 50–55%. A previous myocardial infarction may result in nonfunctioning myocardium that will impair contractility.
  • These variables are important in understanding the pathophysiologic consequences of heart failureand the potential treatments. Furthermore, an appreciation of cardiopulmonary interactions is important in our understanding of heart failure. In the simplest terms, the heart can be viewed as a dynamic pump. It is not only dependent on its inherent properties, but also on what is pumped in and what it must pump against.
  • The exercise intolerance seen with diastolic dysfunction largely results from the impairment of ventricular filling, which elevates left-atrial pressure and pulmonary venous pressure and causes pulmonary congestion. Additionally, inadequate cardiac output during exercise results in poor perfusion of skeletal muscles, especially the leg muscles and the accessory muscles of respiration
  • Patients’ presentation can greatly differ, depending on the chronicity of the disease. For instance, most patients experience dyspnea when pulmonary-artery occlusion pressure exceeds 25 mm Hg. However, the patient with longstanding CHF can tolerate filling pressure up to 40 mm Hg.12

Transcript

  • 1. Congestive Heart Failure
  • 2. Introduction Congestive heart failure (CHF) can result from any functional or structural cardiac disorder that impairs the ventricle’s ability to fill with or eject blood. It remains a clinical diagnosis that is largely based on a careful history and physical examination and supported by ancillary tests such as chest radiograph, electrocardiogram, and echocardiography.
  • 3. Congestive heart failure (CHF) results in pulmonary vascular congestion and reduced cardiac output. should be considered in the differential diagnosis of any adult patient who presents with dyspnea and/or respiratory failure. The measurement of serum brain natriuretic peptide and echocardiography have substantially improved the accuracy of diagnosis.
  • 4. Therapy for CHF restoring normal cardiopulmonary physiology and reducing the hyperadrenergic state. combination of an angiotensin-converting-enzyme inhibitor and slow titration of a blocker. Patients with CHF are prone to pulmonary complications, including obstructive sleep apnea, pulmonary edema, and pleural effusions. Continuous positive airway pressure and noninvasive positive-pressure ventilation benefit patients in CHF exacerbations.
  • 5. Congestive Heart Failure (CHF) Latest Statistic (US) major and growing public health problem in the United States. Approximately 5 million patients in this country have HF, and over 550 000 patients are diagnosed with HF for the first time each year. The disorder is the primary reason for 12 to 15 million office visits and 6.5 million hospital days each year. In 2001, nearly 53 000 patients died of HF as a primary cause. The number of HF deaths has increased steadily despite advances in treatment, in part because of increasing numbers of patients with HF due to better treatment and “salvage” of patients with acute myocardial infarctions (MIs) earlier in life. (AHA,2005)
  • 6. Latest Statistics (Phil population)•In the Philippines, cardiovascular diseases are the mostcommon causes of mortality.•About 77,060 in a 100, 000 populationhave died in thePhilippines due to diseases of the heart.•The prevention of heart failure is an urgent public health needwith national and global implications. (DOH, 2005)
  • 7. Pathophysiology Of Cardiac PerformanceFigure 1
  • 8. Preload the amount of blood presented to the ventricle just before systole. It increases the pressure in the ventricle, which stretches the ventricular wall. Like a rubber band the ventricular muscle fibers need to be stretched ( by blood volume) to produce optimal ejection of blood. Too little or too much muscle fiber stretch decreases the volume of blood ejected. The major factor that determines the preload is a venous return the volume of blood that enters the ventricle during the diastole.
  • 9. Afterload the amount of resistance to the ejection of blood from the ventricle. Afterload inversely related to SV and an increase in afterload causes the ventricle to work harder and may decrease the amount of blood ejected. The major factors that determine afterload are the diameter and distensibility of the great vessels ( aorta and pulmonary artery) and the opening and the competence of the semilunar valves (pulmonic and aortic valves. When the valves open easily the resistance is lower.
  • 10. Contractility The force of contraction, is related to the status of the myocardium. Catecholamines, released by sympathetic stimulation during exercise or from administration of positive inotropic medications, can Increase contractility and SV.
  • 11. Pathophysiology of Congestive Heart Failure  an abnormality in cardiac structure, function, rhythm, or conduction.  Degenerative valve disease, idiopathic cardiomyopathy, and alcoholic cardiomyopathy are also major causes of heart failure.  elderly patients who have multiple comorbid conditions (eg, angina, hypertension, diabetes, and chronic lung disease).  Some common comorbidities such as renal dysfunction are multifactorial (decreased perfusion or volume depletion from overdiuresis), whereas others (eg, anemia, depression, disorders of breathing, and cachexia) are poorly understood.
  • 12. Pathophysiology of Congestive Heart Failure CHF indicates not only an inability of the heart to maintain adequate oxygen delivery; ◦it is also a systemic response attempting to compensate for the inadequacy. The determinants of cardiac output include heart rate and stroke volume (Fig. 1) stroke volume =preload (the volume that enters the left ventricle), contractility, and afterload (the impedance of the flow from the left ventricle).
  • 13. Pathophysiology of Congestive Heart Failure  increased positive pleural pressure can reduce right-atrial pressure (which equals central venous pressure minus pleural pressure), thus reduce ventricular filling.  The cardiac pump is a muscle and will respond to the volume it is given with a determined output. If volume increases, so will the amount pumped out in a normal physiologic state, to a determined plateau; this relationship is described by the Frank- Starling law (Figs. 2 and 3).
  • 14. Pathophysiology of Congestive Heart Failure  Diastolic function is determined by 2 factors: ◦ the elasticity or distensibility of the left ventricle, which is a passive phenomenon ◦ the process of myocardial relaxation, which is an active process that requires metabolic energy  Relaxation of the myocardium occurs in early diastole, and the “untwisting” of the left ventricle is an active process that produces a suction effect that augments left- ventricular filling.  Loss of normal lef tventricular distensibility or relaxation by either structural changes (eg, left-ventricular hypertrophy) or functional changes (eg, ischemia) impairs ventricular filling (preload).
  • 15. PATHOPHYSIOLOGY OFCONGESTIVE HEART FAILURE Fig. 2. The Frank-Starling law of the heart states that as the ventricular volume increases and stretches the myocardial muscle fibers, the stroke volume increases, up to its maximum capacity. After that point, increasing volume increases pulmonary capillary pressure (and pulmonary congestion), without increasing the stroke volume or cardiac output. The mechanism is the length-force relationships of muscle contraction.
  • 16. PATHOPHYSIOLOGY OFCONGESTIVE HEART FAILURE Fig. 3. This series of Frank-Starling curves demonstrates that at any given preload (end-diastolic volume), increases in contractility will increase stroke volume (volume of blood ejected from the ventricle with each beat).
  • 17. Pathophysiology of Congestive Heart Failure  If cardiac output falls, either the heart rate or stroke volume must change in order to maintain perfusion.  If stroke volume cannot be maintained, then heart rate must increase to maintain cardiac output.  It also includes the cardiovascular response to poor perfusion with the activation of the neurohumoral system.
  • 18. Pathophysiology of Congestive Heart Failure  Activation of the renin-angiotensin system attempts to increase preload by stimulating retention of salt and water, increasing vasoconstriction(and, thus, afterload), and augmenting cardiac contractility.  Initially, this response will suffice, but prolonged activation results in loss of myocytes and maladaptive changes in the surviving myocytes and the extracellular matrix.
  • 19. Pathophysiology of Congestive Heart Failure  The stressed myocardium undergoes remodeling and dilation in response to the insult.  This process also has detrimental effects on the functioning of the lungs, kidneys, muscles, blood vessels, and probably other organs.  Remodeling also results in additional cardiac decompensation from complications, including mitral regurgitation from valvular annulus stretching, and cardiac arrhythmias from atrial remodeling
  • 20. Pathophysiology of Congestive Heart Failure  The respiratory care provider often becomes involved with the CHF patient as the elevated end-diastolic pressure leads to pulmonary edema and dyspnea.  The lung provides multiple mechanisms to avoid the consequences of pulmonary edema. Initially, as pressure increases, pulmonary capillaries are recruited and increase capacitance to deal with the added volume.
  • 21. Treatment includes the following:  Nonpharmacologic therapy: Oxygen and noninvasive positive pressure ventilation, dietary sodium and fluid restriction, physical activity as appropriate, and attention to weight gain  Pharmacotherapy: Diuretics, vasodilators, inotropic agents, anticoagulants, beta-blockers, and digoxin
  • 22. A schematic diagramPATHOPHYSIOLOGYOF CHF
  • 23. Non Modifiable factors: Modifiable factors:Gender-female Sedentary LifestyleAge- 55 and above Decreased elasticity of blood vessels and formation of plaques on blood vessels Narrowing of the blood vessels Necrosis and scarring of the vascular endothelium Impediment of blood flow to the body
  • 24. Increased workload of the heart Dilation of ventricles Increased in preloadIncreased stretching of myocardial muscle Excessive stretching of myocardial muscleIneffective cardiac muscle and increase o2 demand ofcardiac muscle Decreased contraction of cardiac muscle Decreased cardiac output and systemic perfusion
  • 25. Activation of neurohormonal patways in order to increase circulating blood vessel Continued neurohormonal stimulation Cardiac remodelling Decreased blood filling Increased stroke volume and decreased cardiac outputInadequate perfusion Increased wall tension
  • 26. Inadequate perfusion Decreased perfusion ofpallor arteries Decreased Increased Deprivation of cardiac muscle cells of nutrients blood flow pulmonary needed for survival to the pressure kidneys Normal balance between oxygen supply and demand is disrupted Fatigue and ischemia Kidneys weakness produce Conversion of aerobic metabolism to hormones anaerobic metalolism Causes reduced contractility Decreased adenosine Salt and water retention Decreased heart Increased lactic acid ability production edema bradycardia Irritation of myocardial cells Chest pain Positive troponin t
  • 27. Increased wall tension Separation of mitral leaflets Increased pulmonary pressure Impaired left ventricular relaxation Increased diastolic pressure exceeding hydrostatic and osmotic pressure in pulmonary capillaries Fluid shifts from circulating blood into the interstitium, bronchioles bronchi and alveoli Pulmonary congestionDecreased lung Fluid trapped inexpansion pulmonary trees dyspnea Bilateral crackles
  • 28. Figure 1. Stages in the Development of Heart Failure/Recommended Therapy by Stage ACEI indicates angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; EF, ejection fraction; FHx CM, family history of cardiomyopathy; HF, heart failur... 2005 WRITING COMMITTEE MEMBERS et al. Circulation 2009;119:e391-e479Copyright © American Heart Association
  • 29. CONGESTIVE HEART FAILURE GUIDELINE Stages in the evolution of heart failure (HF) and recommended therapyby stage. FHx indicates family history of cardiomyopathy; MI, myocardialinfarction; LV, left ventricular; and IV, intravenous.
  • 30. CONGESTIVE HEARTFAILURE GUIDELINE
  • 31. CONGESTIVE HEARTFAILURE GUIDELINE
  • 32. CONGESTIVE HEARTFAILURE GUIDELINE
  • 33. Initial Evaluation incudes the ff: INITIAL EVALUATION 1. H&P, including hx of current &past alcohol&drug use, orthostatic bp changes, , weight&height&BMI 2. 2. Lab teting: CBC, UA, serum Determine type of heart failure based on: electrolytes) BUN, serum >Clinical history creatinine, FBS, lipid profile,liver >EKG and or echocardiogram results fxn tests&TSH >2D echo 3. Assess ability to perform routine &desired activities of daily living 4. 12L ECG 5. Chest x-ray (PA&lateral) Determine stage and Functional Classification Therapy and Education per stage based on AHA guidelines Go back to Initial no evaluation Is patient stable? yes Follow-up at least Controllable as onMANAGEMENT OF every 3-6 months outpatient Admit to hospital CHF IN ACTUAL Return to guideline after discharge from hospital to outpatient care PRACTICE
  • 34. Similarities of Actual Practice and Standard of Care in CHF There is utilization of clinical guideline based on American heart association in managing Congestive Heart Failure. Their management is based on the stage of CHF as indicated in the standard of care. There is both a complete history taking/documentation and rigorous diagnostic procedures in detecting CHF.
  • 35. Similarities of Actual Practice and Standard of Care in CHF The diagnosis of HF is primarily based on signs and symptoms derived from a thorough history and physical examination.
  • 36. Similarities of Actual Practice and Standard of Care in CHF Effects of HF treatment were both monitored with careful measurement of fluid intake and output; vital signs; body weight, determined at the same time each day; clinical signs (supine and standing) and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or active titration of HF medications
  • 37. Similarities of Actual Practice and Standard of Care in CHF In end of life considerations, there are both ongoing patient and family education regarding prognosis for functional capacity and survival for patients with. Most patients hospitalized with severe HF indicate a preference that resuscitation be performed in the event of a cardiopulmonary arrest
  • 38. Differences of Actual Practice from Standard of Care in CHF Practice use of medications where not fully explained in the actual practice
  • 39. Differences of Actual Practice fromStandard of Care in CHF There is absence of exercise training in actual practice. In the guideline, exercise training should be considered for all stable outpatients with chronic HF who are able to participate in the protocols needed to produce physical conditioning. Exercise training should be used in conjunction with drug therapy.
  • 40. Differences of Actual Practice fromStandard of Care in CHF Alternative surgical and mechanical approaches for the treatment of end- stage HF are under development in actual practice. Cardiac transplantation is currently the only established surgical approach to the treatment of refractory HF, but it is available to fewer than 2500 patients in the United States each year.
  • 41. Differences of Actual Practice fromStandard of Care in CHF In actual practice, method of treatment is indicated for general population. Unlike in the standard of care, there is a treatment recommendation/ethical consideration for special population In actual practice, still the management of CHF depends on patient’s cardiologist/general physician, decisions will still be based on the patient. Standard of care in CHF still serves as a guide or backbone of management.
  • 42. Applicability of the Standard of Care in the actual hospital setting It is highly recommended to utilize this guidelines in managing CHF for adult patients. ◦Since, the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980. ◦This effort is directed by the ACCF/AHA Task Force on Practice Guidelines, whose charge is to develop and revise practice guidelines for important cardiovascular diseases and procedures.
  • 43. Applicability of the Standard of Care in the actual hospital setting  The ACCF/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflicts of interest that might arise as a result of an outside relationship or personal interest of a member of the writing committee.
  • 44. Applicability of the Standard of Care in theactual hospital setting  All members of the writing committee, as well as peer reviewers of the document, are asked to provide disclosure statements of all such relationships that might be perceived as real or potential conflicts of interest. Writing committee members are also strongly encouraged to declare a previous relationship with industry that may be perceived as relevant to guideline development.(AHA, 2009). Hence, we can say that it is reliable and a correct practice intended to improve patient care.
  • 45. Applicability of the Standard of Care in the actual hospital setting•The practice guidelines produced are intended to assist healthcareproviders in clinical decision making by describing a range ofgenerally acceptable approaches for the diagnosis, management, orprevention of specific diseases or conditions.•These guidelines attempt to define practices that meet the needs ofmost patients in most circumstances.
  • 46. Applicability of the Standard of Care in theactual hospital setting  These guideline recommendations reflect a consensus of expert opinion after a thorough review of the available, current scientific evidence and are intended to improve patient care.  If these guidelines are used as the basis for regulatory/payer decisions, the ultimate goal is quality of care and serving the patients best interests. The ultimate judgment regarding care of a particular patient must be made by the healthcare provider and patient in light of all of the circumstances presented by that patient. (AHA, 2009)
  • 47. RECOMMENDATIONS HAVE BEEN UPDATED WITH NEW INFORMATION THAT HAS EMERGED FROM CLINICALTRIALS OR OTHER ACCF/AHAGUIDELINE OR CONSENSUS DOCUMENTS
  • 48.  2009 updated recommendation: Measurement of natriuretic peptides (i.e., BNP and NT-proBNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of heart failure is uncertain. Measurement of natriuretic peptides can be useful in risk stratification. (Level of Evidence: A) The 2005 guidelines also recommended measurement of BNP for evaluating patients who present in the urgent care setting with possible heart failure; the 2009 update expanded this recommendation to include the measurement of NT-proBNP. The 2009 update warns that, although elevated natriuretic peptide levels may help confirm a suspected diagnosis of heart failure, the results of this testing alone should not be used to confirm or exclude a heart failure diagnosis.
  • 49.  2009 updated recommendation: Use of ARBs is recommended in patients with current or previous symptoms of heart failure and reduced LVEF who have an intolerance to angiotensin- converting enzyme (ACE) inhibitors. (Level of Evidence: A) 2009 updated recommendation: Maximal exercise testing with or without measurement of respiratory gas exchange is reasonable to facilitate prescription of an appropriate exercise program for patients presenting with heart failure. (Level of Evidence: C)
  • 50. REFERENCE:Hunt, S. et.al. 2013. ACCF/AHA Practice Guideline: FullText 2009 Focused Update Incorporated Into theACC/AHA 2005 Guidelines for the Diagnosis andManagement of Heart Failure in Adults.Circulation.2009; 119: e391-e479.Published online beforeprint March 26,.2009. Retrieved fromhttp://circ.ahajournals.org/content/119/14/e391.full
  • 51. TASK DISTRIBUTION Jaybee Bernandino-latest statistics, pathophysiology Danielle Ann Santiago-actual practice, clinical guideline Cathy Roxas- critique, similarities and differences