1. John Nation RN, MSN Thanks to Nancy Jenkins
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 Ace-Inhibitors-
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

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.

51. Heart Transplant List:
Each patient has a Status ranking
Status 1a: critically ill, hospitalized
Status 1b:require IV medications (inotrops) or heart assist device
Status 2: not hospitalized, do not require IV medications
Status 7: Temporarily inactive

52. Cardiac Transplantation
Surgery involves removing the recipient’s heart, except for the posterior right and left atrial walls and their venous connections
Recipient’s heart is replaced with the donor heart
Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively
Immunosuppressive therapy usually begins in the operating room

53. Cardiac Transplantation
Infection is the primary complication followed by acute rejection in the first year after transplantation
Beyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death
One year survival rate is 85-90%
Three year survival rate is 79%
Local Transplant Story

54. Cardiac Transplantation
Endomyocardial biopsies are obtained from the right ventricle weekly for the first month, monthly for the following 6 months, and yearly thereafter to detect rejection
Endomyocardial Biopsy Video

55. Decreased cardiac output Systolic failure Diastolic failure
Your patient has a normal EF but shows signs of heart failure. Your patient most likely has:
Decreased cardiac output
Systolic failure
Diastolic failure
LV hyypertrophy

56. True or False: Lasix increases preload.

57. Which of the following is associated with left sided failure?
crackles
hypoxemia
tachypnea
Peripheral edema

58. Which of the following are compensatory mechanisms for HF?
Tachycardia
Hypotension
RAAS
LV hypertrophy

59. One of the first signs of Heart failure often is:
Decreased cardiac output
Edema
Fatigue
Atrial fibrillation

60. B. Blood urea nitrogen (BUN) C. Potassium
The nurse is caring for a hospitalized client with heart failure who is receiving captopril (Capoten) and spironolactone (aldactone). Which lab value will be most important to monitor?
A. Sodium
B. Blood urea nitrogen (BUN)
C. Potassium
D. Alkaline phosphatase (ALP)