Heart Failure

1. Heart Failure By Robert Reynoso, RN, CEN Special Thanks to William Dubois, RN, CEN

2. OBJECTIVES • The Registered Nurse (RN) will understand cardiac anatomy & physiology • The RN will be able to identify Heart Failure (HF) risk factors and its pathophysiology • The RN will understand current medical and nursing management

3. WHY HEART FAILURE? Heart Failure is a significant medical, economic and social aspect of healthcare often not given proper consideration and care It is also one of the top conditions causing readmission. Centennial Hills is in the midst of attaining Heart Failure Center status

4. PREVALENCE • According to American Heart Association (AHA in 2006 • Adults 20 years and older • 5.7 Million (3.2 Million Male) • Heart Failure (HF) incidence approaches 10 per 1,000 people aged 65 and older

5. INCIDENCE • From Circulation. 2002;106:3068–3072 • 75% of HF cases have antecedent hypertension • At age 40, lifetime risk of developing HF for both men and women is one in five • At age 40, lifetime risk of HF occurring without antecedent heart attack is 1 in 9 for men and 1 in 6 for women • The lifetime risk doubles for people with blood pressure (BP) greater than 160/90 mm Hg compared to those with BP less than 140/90 mm Hg.

6. RISK FACTORS • Hypertension (HTN) is a very common risk factor for HF that has contributed to a large proportion of heart failure cases among the study’s participants (JAMA. 1996;275:1557–1562.) • Study of the predictors of HF among women with coronary heart disease found that diabetes was the strongest risk factor (Circulation. 2004;110:1424–1430.) • Prevalence of diabetes is increasing among older persons with HF • Diabetes is a significant independent risk factor for death in these individuals • Researchers found that the odds of having diabetes for those first diagnosed with HF in 1999 was nearly four times higher than for those diagnosed 20 years earlier (Am J Med. 2006;119:591-599.)

7. MORTALITY • 2005 total deaths from HF: 292, 214 • 58,933 additionally listed as underlying cause • Based on the 44-year follow-up of the National Heart Lung Blood Institute's (NHLBI) Framingham Heart Study and 20-year follow-up of the offspring cohort: • 80% of men and 70% of women under age 65 who have HF will die within 8 years • After HF is diagnosed, survival is poorer in men than in women, but less than 15 percent of women survive more than 8–12 years. The one-year mortality rate is high, with one in five dying • In people diagnosed with HF, sudden cardiac death occurs at six to nine times the rate of the general population

8. HOSPITAL DISCHARGES & COST • Hospital discharges for HF rose from 877,000 in 2005 to 1,106,000 in 2006 • Increase of 171% • What do you think the estimated direct and indirect cost of HF in the United States was for 2009?

9. POP QUIZ • According to the AHA & International Monetary Fund, the USA spends more on HF than the Gross Domestic Product (GDP) of:

10. ANSWER • 100 countries have GDP’s less than what the USA spent on HF in 2009 • The estimated direct and indirect cost of HF in the United States for 2009 is $37.2 BILLION

11. PHYSICAL INACTIVITY New Remote Control Can Be Operated By Remote TOKYO—Television watching became even more convenient this week with Sony's introduction of a new remote-controlled remote control.

12. SMOKING

13. HYPERLIPIDEMIA Report: Meat Now America's No. 2 Condiment • CHICAGO—Though once defined as just a stand-alone meal, meat has risen quickly up the ranks to become the nation's second most popular condiment, according to a study released by the U.S. Department of Agriculture.

14. OVERWEIGHT & OBESITY So-Called Obese Pets Held To Unrealistic Body Standards CHICAGO—To the casual eye, Tippy might appear to be a regular Labrador. He loves sunbathing at the park, watching squirrels, and getting loads of attention from passersby.

15. DIABETES MELLITUS

16. ISCHEMIC HEART DISEASE

17. ILLICIT DRUG ABUSE & ETOH

18. DILATED CARDIOMYOPATHY

19. CONNECTIVE TISSUE DISEASES

20. VALVULAR HEART DISEASE

21. MYOCARDITIS

22. AMYLOIDOSIS

23. SLEEP APNEA

24. PHARMACOLOGICS

25. LAYERS OF THE HEART

26. CARDIAC ANATOMY

27. THE CARDIAC PACEMAKER

28. STROKE VOLUME (SV) • Volume of blood pumped from the heart with each beat. • Cardiac Output (CO) x 1000 /Heartrate (HR) • Normal Range: 60-100mL/beat

29. CARDIAC OUTPUT (CO) • Volume of blood being pumped by the heart in a minute • CO=Stroke Volume (SV) x Heartrate (HR) • Normal Range: 4-8 L/min

30. Mean Arterial Pressure (MAP) • Average arterial pressure during a single cardiac cycle • SBP + (2 x DBP) / 3 • Normal Range: 70-105 mm/Hg

31. EJECTION FRACTION • Fraction of blood pumped out of a ventricle with each heart beat. Normal: 60-75%. • Stroke volume varies by size of patient (adult versus peds.) • Applies to both the right and left ventricles • One can speak equally of the left ventricular ejection fraction (LVEF) and the right ventricular ejection fraction (RVEF). • Without a qualifier, the term ejection fraction refers specifically to that of the left ventricle

32. FRANK-STARLING LAW OF THE HEART • States that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) • As the heart fills with more blood than usual, the force of the muscular contractions will increase. • This is a result of an increase in the load experienced by each muscle fiber due to the extra blood entering the heart. • The stretching of the muscle fibers increases the affinity of troponin C for calcium, causing a greater number of cross-bridges to form within the muscle fibers; this increases the contractile force of the cardiac muscle.

33. BOILED DOWN • Basically, preload is stretch. The amount of volume being returned to the right side of the heart from systemic circulation. • Afterload is squeeze. The amount of resistance the left side of the heart has to overcome in order to eject blood.

34. PRELOAD • Preload is the initial stretching of the cardiac myocytes prior to systole.  Preload, therefore, is related to the sarcomere length. Because sarcomere length cannot be determined in the intact heart, other indices of preload are used such as ventricular end-diastolic volume or pressure. • For example, when venous return is increased, the end-diastolic pressure and volume of the ventricle are increased, which stretches the sarcomeres (increases their preload). • Increased preload increases stroke volume, whereas decreased preload decreases stroke volume by altering the force of contraction of the cardiac muscle.

35. PRELOAD INCREASED BY • Increased central venous pressure • Reduced heart rate • Valvular regurgitation • Increased aortic pressure • Ventricular systolic failure DECREASED BY • Decreased central venous pressure • Increased heart rate • Inflow valvular stenosis • Atrial arrhythmias • Ventricular diastolic failure

36. AFTERLOAD • Afterload can be thought of as the "load" that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure. • Afterload is increased when aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis, and by ventricular dilation. When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.

37. AFTERLOAD INCREASED BY • Hypertension • Vasoconstriction

38. PATHOPHYSIOLOGY • HF is caused by any condition which reduces the efficiency of the heart through damage or overloading. Over time these increases in workload will produce changes to the heart itself. Examples of conditions: • AMI (in which the heart muscle is starved of oxygen and dies) • HTN(which increases the force of contraction needed to pump blood) • Amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen).

39. PATHOPHYSIOLOGY • Heart rate increases, stimulated by more sympathetic activity in order to maintain cardiac output. • Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion but places further strain on the myocardium increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease

40. PATHOPHYSIOLOGY • Hypertrophy of the myocardium means the heart muscle fibers increase in size in an attempt to improve contractility. • Increased stiffness • Decreased ability to relax during diastole • Enlargement of the ventricles contributes to the enlargement and spherical shape of the failing heart. • The increase in ventricular size also causes a reduction in SV due to mechanical and contractile inefficiency.

41. PATHOPHYSIOLOGY • General effect is one of reduced CO and increased strain on the heart. • This increases the risk of cardiac arrest and reduces blood supply to the rest of the body. • In chronic HF, the reduced CO causes a number of changes in the rest of the body.

42. THE BRAIN AND HF • When arterial blood pressure falls, baroreceptors in the carotid sinus and aortic arch are DE-stimulated • The brain increases sympathetic activity, releasing catecholamines into the blood stream. • Catecholamines: • Bind to alpha-1 receptors resulting in systemic arterial vasoconstriction • Restore BP but also increases total peripheral resistance, increasing the workload of the heart • Bind to beta-1 receptors in myocardium increasing the heart rate, making contractions more forceful and attempting to increase CO • Ultimately increasing the amount of work the heart has to perform

43. THE KIDNEYS AND HF • Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (ADH), which causes fluid retention by the kidneys • This increases the blood volume and blood pressure. • Reduced perfusion to the kidneys stimulates the release of renin –which catalyzes the production of the potent vasopressor angiotensin. • Angiotensin and its metabolites cause further vasoconstriction and stimulate increased secretion of aldosterone from the adrenal glands. • This promotes salt and fluid retention which increases the blood volume.

44. THE HEART AND HF B-type natriuretic peptide (BNP) • A 32-amino-acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of myocytes in the ventricles • Decreases systemic vascular resistance • Decreases central venous pressure • Increases natriuresis (gets rid of salt)

45. EDEMA & FLUID • Increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. • Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries • This shifts the balance of forces in favor of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue

46. RIGHT SIDED FAILURE • Failure of the right ventricle leads to congestion of systemic capillaries. • Leads to excess fluid accumulation (edema & anasarca) • Usually affects the dependent parts of the body first • (Foot and ankle swelling in people who are standing up and sacral edema in people who are predominantly lying down) • Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. • In severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and hepatomegaly (enlargement of the liver) may develop • Significant liver congestion may result in discomfort or impaired liver function. Jaundice and coagulopathy may occur.

47. SIGNS • Exam can reveal: • Pitting peripheral edema • Ascites • Hepatomegaly. • Jugular venous distention

48. LEFT SIDED FAILURE • Failure of the left ventricle causes congestion of the pulmonary vasculature and predominantly respiratory symptoms • Dyspnea on exertion • In severe cases, at rest • Increasing dyspnea while supine (orthopnea)may occur • Often measured in the number of pillows required to lie comfortably • In severe cases, the patient may resort to sleeping while sitting up • Paroxysmal nocturnal dyspnea, a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep • Easy fatigue and exercise intolerance are also common complaints • Compromise of left ventricular forwardfunction may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest

49. SIGNS & SYMPTOMS • Common respiratory signs are: • Tachypnea and increased respiratory effort • Rales or crackles heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema • Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema. • Additional signs indicating left ventricular failure include: • Heart murmurs which may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

50. SYSTOLIC DYSFUNCTION • Heart failure caused by systolic dysfunction is “Pump Failure” • Characterized by a decreased ejection fraction (less than 40%) • Ventricular contraction is lessened and inadequate for creating an adequate SV (inadequate CO) • In general, this is caused by dysfunction or destruction of cardiac myocytes. Myocytes can be damaged by: • Inflammation (myocarditis) • Infiltration (amyloidosis) • Toxins and pharmacological agents (such as ethanol, cocaine, and amphetamines) cause intracellular damage • Congenital diseases such as Duchenne muscular dystrophy (molecular structure of individual myocytes is affected) • Ischemia causing infarction and scar formation. • After AMI, dead myocytes are replaced by scar tissue affecting the function of the myocardium. On echocardiogram, this is seen as abnormal or absent wall motion.