CHF

1. CHF Joan Goss BSN, RN Clinical Educator Union Memorial Heart Institute

2. Objectives By the end of this session the participant will be able to: • Define heart failure • Discuss common causes of heart failure • Describe the signs and symptoms of heart failure • Describe treatment options for heart failure patients. • Apply evidenced based nursing interventions when planning care for the CHF patient. • Discuss common complications related to heart failure

3. Definition “Clinical presentation of impaired cardiac function in which one or both ventricles are unable to maintain an output adequate to meet the metabolic demands of the body”.

4. Effects of CHF • 37 billion dollars per year spent on inpatient and outpatient care. • Over 5 million American suffer from CHF • 550,000 new cases are diagnosed each year • Most frequent admission to the hospital for Medicare patients. • Only 20-39% of people diagnosed with heart failure survive 10 years. (Blum 2005)

5. Coronary artery disease Dilated cardiomyopathy Hypertrophic cardiomyopathy Restrictive Cardiomyopathy Infiltrative disorders Hypertension Aortic stenosis Pulmonary hypertension Valvular disease Congenital heart disease Arrhythmias Cardiac tamponade Renal failure High output states such as thyrotoxicosis, anemia. (Blum 2005) Causes of Heart Failure

6. Pathophysiology of Heart Failure

7. Effects of Neurohormonal Activation Sympathetic: Increased heart rate, increased contractility, increased cardiac output and stroke volume, increased myocardial oxygen consumption. RAAS: Increased arterial vasoconstriction, increased systemic vascular resistance, increased renal vasoconstriction, sodium and water retention. (Blum 2005)

8. Neurohormones • Initial effects are intended as helpful. • With continued stimulation: Pulmonary congestion Anasarca Exacerbation of pump dysfunction Increase in cardiac energy expenditure

9. Counter-regulatory mechanism • Natriuretic peptides BNP: Brain natriuretic peptide Released from the ventricles in response to increased volume and pressure. Exerts the following effects: Natriuresis: excretion of sodium in the urine (where sodium goes water follows) decreasing circulating volume. Vasodilation: Decreases venous return to the heart.

10. BNP • Can be measured in serum plasma: referred to as the BNP assay. • Helps to differentiate pulmonary from cardiac causes of dyspnea • Can help to guide HF therapy • Normal BNP is 0-100 pg/ml. • BNP levels above 100 pg/ml indicate heart failure. • The higher the BNP level, the greater the severity of heart failure.

11. BNP assay • Pitfalls: Levels may be elevated in other conditions such as stroke, severe sepsis, septic shock, hyper-thyroidism, and subarachnoid hemorrhage.

12. Further Classifications of Heart Failure • Can be further classified as: Right vs. Left sided Systolic vs. diastolic Forward vs. backward flow

13. Pathophysiology Left sided systolic dysfunction: • Decreased left ventricular contractility impairing the forward flow of blood into the circulatory system. • EF is less than 45% • In an attempt to compensate, the left ventricle dilates and HR increases to maintain CO. • Decreased renal perfusion initiates the Renin-Angiotensin-Aldosterone system, cortisol release, and release of epinephrine and norepinephrine. (Lessig 2006)

14. Systolic dysfunction • RAAS, catecholamine and cortisol release lead to vasoconstriction, increased HR, and sodium re-absorption in the distal tubules of the kidney. • End result is fluid overload. • Long term activation can result in changes to the structure of the heart muscle itself. These changes are described as cardiomyopathy. (Lessig 2006)

15. Dilated cardiomyopathy: ventricular chamber dilates , thins, and changes from an elliptical shape to a more spherical shape. This reduces contractile function and impairs emptying. (Lessig 2006) Dilated cardiomyopathy

16. Ischemic cardiomyopathy • Results in oxygen levels that are inadequate to meet the metabolic demands of the cardiac muscle cells. • Occurs with CAD: may be acute or chronic • Formation of ATP is affected • Calcium, sodium, and potassium pumps fail • Leads to decreased contractility and dysrrhythmias. (Lessig 2006)

17. Ischemic cardiomyopathy • If ischemia continues: heart muscle dies • Dead muscle cells are replaced with scar tissue • Scar tissue cannot participate in contraction so cardiac output declines. (Lessig 2006)

18. Myocarditis • Frequently acute onset • Can be caused by bacteria, viruses, idiopathic causes, thyroid dysfunction, HIV, or hemochromatosis. • Dysfunction results from inflammation of the heart muscle. • Inflamed cardiac cells do not contract well • Leads to decreased cardiac output. • Severity can range from cardiogenic shock to mild physical limitations. (Lessig 2006)

19. Ischemic heart disease MI Myocardial stunning CAD Idiopathic dilated cardiomyopathy Myocardial contusion Aortic insufficiency Arrhythmias Post pump syndrome Myocarditis Infectious, bacterial/viral Rheumatic fever Drug abuse Electrolyte disorders Diabetes Thyroid disease Negative inotropic drug (Lessig 2006) Causes of LV systolic dysfunction

20. Anxiety Dizziness Orthopnea Dyspnea/dyspnea on exertion Diaphoresis/palpitations Hypoxia Elevated PA pressures Nocturia Nursing Assessment Tachypnea Rales, rhonci, wheezes S3 gallop Tachycardia hypotension Low SaO2 (Lessig 2006) Signs and symptoms of LV systolic dysfunction

21. Left ventricular diastolic dysfunction • Occurs when the heart muscle becomes stiff and thickened. • Cannot relax enough to accept adequate blood volume • EF remains greater than 45% • Edema especially in the periphery but can also have lung congestion • Can occur independently or in conjunction with systolic dysfunction (called mixed failure) (Morton, Fontain, Hudak Gallo, 2005)

22. Hypertrophic CM The heart muscle becomes thickened with increased muscle mass and is unable to relax to accept blood. EF remains normal Most often caused by long standing hypertension Can also be caused by aortic stenosis, mitral stenosis, or primary pulmonary hypertension. (Morton, Fontain, Hudak Gallo, 2005) Cardiomyopathy

23. Failure of the right ventricle to pump adequately into the pulmonary circulation. Most common cause of right heart failure is left heart failure. Can exist in the presence of normal left ventricular function. Can also result from primary pulmonary hypertension (cor pulmonale) Acute onset of right heart failure is often caused by a pulmonary embolus. Right sided heart failure

24. Increased fatigue Splenomegaly Hepatomegaly Dependent pitting edema Ascites/Weight gain Abdominal pain Oliguria Hypotension Venous distention (JVD) Hepatojugular reflux S3/S4 heart sounds Elevated central venous pressures. (Lessig 2006) Signs of Right Heart Failure

25. Two Classification Systems • NYHA Functional Classification • ACC/AHA Stages

26. NYHA Classification

27. ACC/AHA Stages

28. Diagnostic Studies • LAB: BNP, C-reactive protein, HCT/Hgb (anemia), electrolytes, TSH, BUN/Creatinine, LFTs (right-sided), Cardiac enzymes, HIV. • CXR: pulmonary edema, pleural effusions, heart enlargement. • EKG: Non-specific changes, arrhythmias, ischemic changes. (Lessig 2006)

29. Diagnostic Studies • Echocardiogram: Chamber size, muscle thickness, thrombi, systolic/diastolic function, valvular disease. • Radionuclide imaging: Perfusion, chamber volumes. • CT/MRI: structural abnormalities, tumors, pericardial disease. • Cardiac catheterization: coronary anatomy, chamber pressures, contractility, valvular problems and cardiac defects. (Lessig 2006)

30. Goals for patient care • Heart failure symptoms are relieved • Hemodynamic parameters are optimized • Fluid balance is corrected/edema resolved • Arrhythmia complications are prevented (Lessig 2006)

31. Nursing Management • Reverse Trendelenberg positioning • Prevention of DVT: anticoagulation therapy, ROM, anti-thrombotic stockings and SCDs • Skin integrity • Pain Management • Nutrition: Intake and Outputs extremely important !!!! Fluid and Sodium restrictions Daily weights (Lessig 2006)

32. Pharmacology (McConaghy and Smith 2004)

33. Medications • Diuretics: Lasix Used to control fluid volume Decreases preload Produce rapid symptom relief Useful in management of acute states Nursing: Evaluate patient response (I/O) Decreased edema, decreased rales, increased SaO2? Monitor for electrolyte imbalances Impaired renal function Hypovolemia

34. Question The following are all adverse effects of Lasix except: • Renal dysfunction • Hypotension • Dehydration • Hyperkalemia

35. Inotropic agents • In acute CHF: Dobutamine/Milrinone Increases contractility Decreases afterload and improves CO Dopamine Increases renal perfusion and assists in diuresis at low doses.

36. ACE Inhibitorscaptopril,lisinopril, enalapril • First line treatment for heart failure patients • This is a required medication for all patients with systolic dysfunction! • If patient unable to tolerate ACE-I try ARBs • If unable to tolerate both, documentation must occur as to why the patient is not receiving. • Slows progression of remodeling • Interrupts the conversion of angiotensin I II • Decreases afterload, reducing the workload on the heart

37. Adverse effects of ACE-I • Hypotension • Renal dysfunction • Hyperkalemia • Cough • Rash • Angioedema • Taste disturbance

38. When not to use ACE-I • Large increase in creatinine after starting ACE-I therapy • History of angioedema • Moderate to severe aortic insufficiency • Pregnancy • Intolerable side effects

39. ARBsvalsartan, candasartan, losartan, cozaar • Angiotensin Receptor Blockers Blocks angiotensin II receptors preventing effects on heart and blood vessels Can be used in patients that cannot tolerate ACE-I Side-effects not as extensive: Hypotension Increased serum creatinine

40. Beta-blockersmetoprolol, coreg • Block the sympathetic system • Historically contraindicated for patients with systolic dysfunction, but has now been found to improve ejection fraction. • Used for HR and BP control in diastolic dysfunction • Studies have shown reduced morbidity and mortality when used post OHS

41. Beta-Blocker side-effects • Dizziness • Fatigue • Probably due to concomitant alpha blockade • May need to adjust diuretic and ACE-I dosages • Watch for bradycardia and hypotension

42. Calcium Channel blockerscardizem, norvasc, nifedipine • Contraindicated in systolic dysfunction…why? • In diastolic failure: decreases heart rate and BP, reduces myocardial ischemia • Not a primary treatment…used when other medications are ineffective.

43. Digoxin • Used in heart failure patients with a history of atrial fibrillation or flutter • Decreases the symptoms of heart failure and improves exercise tolerance • Does not decrease mortality • Can be ordered for patients with frequent readmissions despite maximum therapy • Contraindicated in diastolic failure…why? • Watch for digoxin toxicity

44. Digoxin toxicity • Reduce dose in patients with renal disease or who are taking amiodarone • Blood levels should remain less than 2 ng/ml • Watch for fatigue, anorexia, nausea, vomiting, arrhythmias, heart blocks, bradycardia, green or yellow vision disturbances.

45. Nitratesisosorbide dinitrate/monotrate(isordil, imdur) • Venodilators • Used to decrease preload • Coronary vasodilators: dilate coronaries to increase cardiac perfusion • Helps alleviate orthopnea and dyspnea on exertion.

46. Natrecor • Recombinant human B-type natriuretic peptide (hBNP) • Produces a dose dependant reduction in PCWP and systemic arterial pressure in patients with heart failure. • Results in decreased dyspnea. • Some physicians are reluctant to use due to several studies that indicate renal dysfunction following administration (probably due to hypotension and decreased renal perfusion). • BNP assay results will be elevated with Natrecor therapy.

47. BP management • Remember, in heart failure the lowest blood pressure that is tolerated is optimal (as long as the kidneys are perfusing). • Having said this, there is one exception…..

48. Aortic stenosis • When the aortic valve becomes stenotic, it does not open normally. • The ventricles need to “push” blood out through a narrowed valve. • Blood pressure after the valve must be kept higher to counteract the valve resistance

49. Non-pharmacologic management Sodium restricted diet is imperative -no canned soups or vegetables Alcohol use should be stopped because it is a cardiac depressant Exercise programs should be initiated to increase stamina (low level) Weight lifting is not recommended because it increases afterload Weigh each day and report an increase of 3 or more pounds. Goal is to manage fluid overload prior to needing hospitalization (Morton, Fontain, Hudak Gallo, 2005)

50. CHF management • When to call the MD • S/S of worsening heart failure • Importance of keeping appointments • Vitamin supplements • Flu and pneumonia vaccines • Advance directives • Avoidance of NSAIDs