Heart Failure

1. Heart Failure John Nation RN, MSN Thanks to Nancy Jenkins

2. Overview: • Incidence/ Definition • A & P Review • Pathophysiology • Types of Heart Failure • Complications • Treatments • Nursing Care • Devices • Heart Transplant

3. Incidence/ Definition Heart Failure- clinical condition involving impaired cardiac pumping Incidence: • 5 million people in US have HF • 470,000 new cases each year • 1 in 100 adults has HF • Most common reason for hospital admission in adults >65 years old

4. A & P Review:

5. What Causes Heart Failure? • Coronary Artery Disease (CAD) • Myocardial Infarction • Dysrhythmias • Pulmonary Emboli • Hypertension • Congential Heart Disease • Cardiomyopathy • Valve problems • Endocarditits • Myocarditis • Idiopathic (don’t know!)

6. Key Terms: • Cardiac Output- Stroke volume x heart rate • Normal value is 4-8 Liters/min • Stroke Volume- Amount of blood pumped from the heart with each heart beat • Preload- the volume of blood in the ventricles at the end of diastole, before the next contraction. • Afterload- the peripheral resistance that the left ventricle pumps against

7. Types of Heart Failure: Systolic Heart Failure: • Most common type • The ventricles are not providing adequate contractions (it’s not pumping well enough) • Defined primarily in terms of the left ventricular ejection fraction (EF) • Ejection Fraction (EF)- percentage of total ventricular filling volume that is ejected during contraction. Normal EF is 55-70%.

8. Ejection Fraction:

9. Types of Heart Failure (Cont’d): Diastolic Heart Failure: • Impaired ability of the heart to relax and fill during diastole • Causes decreased stroke volume (and therefore decreased cardiac output • Caused largely by stiff or noncompliant ventricles • Diagnosis based on heart failure symptoms with normal ejection fraction. • Often caused by hypertension and myocardial fibrosis

10. Types of Heart Failure (Cont’d): Systolic and Diastolic Heart Failure • Low ejection fraction and poor relaxing (and thus poor filling) of ventricles • Often characterized by biventricular failure • Often seen with dilated cardiomyopathies

11. Types of Heart Failure (Cont’d): Left-Sided Heart Failure: • Most common form • Blood backs up into left atrium and pulmonary veins • Causes pulmonary congestion/ edema Right-Sided Heart Failure: • Primary cause is left-sided heart failure • Blood backs up into venous circulation • Causes hepatomegaly, splenomegaly, peripheral edema

12. Cor Pulmonale:

13. How the Body Responds: • Remember, a decrease in stroke volume leads to a decrease in cardiac output. • Body attempts to increase cardiac output: • Sympathetic Nervous System • Neurohormonal Response • Dilation of chambers of the heart • Hypertrophy • Natriuretic peptides

14. The Body’s Response: Sympathetic Nervous System: • Release of catecholamines (epinephrine and norepinephrine) • Causes increased heart rate & increased contractility • Increases workload on heart • Increases oxygen need of heart

15. The Body Responds (Cont’d): Neurohormonal Response: • As CO decreases, blood flow to kidneys decreases: • Causes activation of renin-angiotensin-aldosterone system (RAAS) • RAAS causes sodium and water retention, peripheral vasoconstriction, increased BP • Low CO decreases cerebral perfusion pressure: • Posterior pituitary secretes more antidiuretic hormone (ADH) • ADH causes more fluid retention and production of endothelin. • Endothelin causes arterial vasocontriction & increased contractility of heart muscle

16. The Body Responds (Cont’d): Neurohormal Response (Cont’d): • Due to various types of cardiac injury (ie MI), proinflammatory cytokines are released. • Cause cardiac hypertrophy, pumping dysfunction, and death of cells in the heart muscle • Over time, this process can lead to a systemic inflammatory response that further damages the heart

17. The Body Responds (Cont’d): Dilation: • Chambers of the heart get larger • Increase in stretch of muscle fibers due to increase in blood volume • The greater the stretch, the greater the force of contraction (Frank-Starling Law) • Initially, causes increase in cardiac output. After time, muscle fibers are overstretched and contraction decreases

18. The Body Responds (Cont’d): Hypertrophy: • Increase in muscle mass of heart • Increases contractility at first • However, hypertrophic muscle doesn’t work as well, needs more oxygen, greater risk for rhythm problems, and has poor circulation

19. The Body Responds (Cont’d):

20. Hypertrophy vs Dilation

21. The Body Responds (Cont’d): Natriuretic Peptides: • Atrail natriuretic peptide (ANP) & b-type natriuretic peptide (BNP) • Hormones produced by the heart that promote vasodilation (decreasing preload and afterload) • Increase glomerular filtration rates • Block effects of RAAS

22. Clinical Manifestations: Acute Decompensated Heart Failure: • Often presents as pulmonary edema • Often associated with CAD/ MI • Pale, anxious, dyspnea, possibly cyanotic, crackles, wheezing, rhonhi, blood in sputum, increased HR, S3 heart sound

23. Clinical Manifestations (Cont’d): Before treatment After treatment

24. Clinical Manifestations (Cont’d): Chronic Heart Failure: • Depends on right vs left sided failure • Often has signs/ symptoms of biventricular failure • Fatigue • Dyspnea • Nocturnal Dyspnea • Tachycardia • Edema • Nocturia • Chest pain • Weight changes • Behavioral changes

25. Clinical Manifestations (Cont’d):

26. Complications: • Hepatomegaly • Dysrhythmias • Pleural Effusion • Thrombus • Renal Failure • Cardiogenic Shock

27. Classification: NYHA Classifications: • Class I- No limitation of physical activity. Ordinary activity does not cause fatigue, dyspnea, palpitations, or anginal pain • Class II- Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in fatigue, dyspnea, palpitations, or anginal pain • Class III- Marked limitation of physical ability. Usually comfortable at rest. Ordinary activity causes fatigue, dyspnea, palpitations, or anginal pain • Class IV- Inability to carry on any physical activity without discomfort. Symptoms may be present at rest.

28. Classification (Cont’d): ACC/ AHA Stages of Heart Failure: • Stage A- Patients at high risk for developing left ventricular dysfunction because of conditions that are strongly associated with development of HF • Stage B- Patients who developed structural heart disease that is strongly associated with development of HF but who have no symptoms • Stage C- Patients who have current or prior symptoms of HF associated with underlying structural heart disease • Stage D- Patients with advanced structural heart disease and marked symptoms of HF at rest despite maximized medical therapy and who require specialized interventions

29. Diagnostic Tests: • History and Physical • CBC, BMP, cardiac enzymes, liver function tests, BNP, PT/INR • Chest x-ray • 12- lead ECG • Echocardiogram • Nuclear imaging studies • Stress testing • Hemodynamic monitoring • Heart catheterization

30. Echocardiogram: Transesophageal echocardiogram TEE Echocardiogram Video

31. Treatment Goals: • Decreasing Intravascular Volume- decreases venous return, decreases preload, more efficient contraction and increased cardiac output • Decreasing Preload- vasodilator, positioning • Decreasing Afterload- decreases pressure against which LV must pump • Increasing Contractility- inotropes increase cardiac output

32. Drug Therapy: Diuretics: reduce preload • Furosemide (Lasix)- PO or IV, loop diuretic. • Spironolactone (Aldactone)- PO, potassium sparing diuretic • Metolazone (Zaroxolyn)- PO, when extra diuresis necessary • Ace-Inhibitors- • lisinopril • first line therapy in chronic HF • block conversion of angiotensin I to angiotensin II, • decrease aldosterone • Decrease afterload. Increase cardiac output.

33. Drug Therapy (Cont’d): Vasodilators: • Nitrates- directly dilate vessels, decrease preload, vasodilate coronary arteries. • Nitroprusside (Nipride)- reduces preload and afterload • Nesiritide (Natrecor)- arterial and venous dilation B- Blockers- Carvedilol (Coreg), Metoprolol (Lopressor) • Block negative effects of SNS system (such as HR) • Can reduce myocardial contractility • Improve patient survival

34. Drug Therapy (Cont’d): Positive Inotropes: Increase contractility • Digoxin- increases contractility, decreases HR • Watch for hypokalemia • Reduces symptoms, but not shown to prolong life • Dopamine • Dobutamine • Milrinone (Primacor) Angiotensin II Receptor Blockers (ARBs) • Mostly for patients unable to tolerate Ace Inhibitors • Similar effects to Ace Inhibitors Isosorbide dinitrate and hydralazine (BiDil)- for African Americans with HF.

35. Collaborative Care: • Treat underlying cause (if possible) • Oxygen therapy PRN • Cardiac rehab • Daily weights • Drug therapy education • Sodium restriction • Strict Input/ output • Symptom education • Home health • Specialty clinics

36. Discharge Teaching- JCAHO- • Weight Monitoring • Medications • Activity • Diet • What to do if symptoms worsen • Follow-up

37. Nursing Diagnosis • Activity intolerance • Decreased cardiac output • Fluid volume excess • Impaired gas exchange • Anxiety • Deficient knowledge

38. Decreased cardiac output • Plan frequent rest periods • Monitor VS and O2 sat at rest and during activity • Take apical pulse • Review lab results and hemodynamic monitoring results • Fluid restriction- keep accurate I and O • Elevate legs when sitting • Teach relaxation and ROM exercises

39. Activity Intolerance • Provide O2 as needed • practice deep breathing exercises • teach energy saving techniques • prevent interruptions at night • monitor progression of activity • offer 4-6 meals a day

40. Fluid Volume Excess • Give diuretics and provide BSC • Teach side effects of meds • Teach fluid restriction • Teach low sodium diet • Monitor I and O and daily weights • Position in semi or high fowlers

41. Knowledge deficit • Low Na diet • Fluid restriction • Daily weight • When to call Dr. • Medications

42. Treatment: Devices: Cardiac Resynchronization Therapy (CRT): • Utilizes biventricular pacing • Coordinates right and left ventricle contractility • Normal electrical conduction increases CO • For patients with Class III and IV HF • Patients with HF caused by ischemia and EF <35% may need implantable cardiac defibrillator (ICD) as well due to risk of dysrhythmias

43. Intraaortic Balloon Pump (IABP): • Temporary circulatory assistance • Reduces afterload • Improves coronary blood flow • Helps aortic diastolic pressure • IABP Video

44. Ventricular Assist Devices (VAD): • Circulatory device that provides cardiac output in addition to that of native heart • Usually takes blood from left ventricle then pumps to the aorta • Many different types, primarily Heartmate II and PVAD • Heartmate II much easier to transport, continous flow to put blood out to body • VAD Patient Video • Heartmate II Thoratec Video(2 min 45 sec)

45. PVAD/ IVAD

46. Heartmate II:

47. VADs (Cont’d) • Either bridge to transplant or as destination therapy • Must meet criteria for implantation • Be able to manage pump at home (in many cases) • Require anticoagulation therapy

48. Heart Transplantation: • First performed in 1967 • Over 2000 each year in US • Long wait time, not enough hearts • From harvest to transplantation there is a 4-6 hr maximum time

49. Heart Transplantation (Cont’d): Absolute Indications: • Cardiogenic shock • Dependence on IV inotropes (ie dobutamine) • Severe cardiac ischemia not able to be fixed by PCI or CABG • Symptomatic, refractory life threatening dysrhythmias (ie V-tach) Relative Indications: • Persistent fluid overload despite medical therapy • Persistent unstable angina

50. Heart Transplantation (Cont’d): Possible exclusion criteria (exceptions for some patients/ differs by center): • >65 yrs old • Severe pulmonary HTN (irreversible) • Irreversible kidney or liver disease not explained by HF • Severe chronic lung disease • Active infection • Cancer in last 5 yrs • Other conditions as well, this is guiding list.