1. Focus on Heart Failure (Relates to Chapter 35,
“Nursing Management: Heart Failure,” in the textbook)

2. Heart Failure Syndrome involving impaired cardiac pumping
Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs
Characterized by
Ventricular dysfunction
Reduced exercise tolerance
Diminished quality of life
Shortened life expectancy

3. Heart Failure (Cont’d)
Associated with long-standing hypertension and coronary artery disease
Affects about 5 million people in the United States
The most common reason for hospitalization in adults >65 years of age

4. Etiology and Pathophysiology
Primary risk factors
Coronary artery disease (CAD)
Advancing age
Contributing risk factors
Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent

5. Systolic vs. Diastolic Heart Failure
Systolic failure is the most common cause
Hallmark finding: Decrease in the left ventricular ejection fraction (EF)
Caused by
Impaired contractile function (e.g., MI)
Increased afterload (e.g., hypertension)
Cardiomyopathy
Mechanical abnormalities (e.g., valve disease)

6. Etiology and Pathophysiology (Cont’d)
Diastolic failure
Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO
Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, normal ejection fraction (EF)

7. Etiology and Pathophysiology (Cont’d)
Diastolic failure
Caused by
Left ventricular hypertrophy from chronic hypertension
Aortic stenosis
Hypertrophic cardiomyopathy
Isolated right ventricular diastolic failure from pulmonary hypertension

8. Mixed systolic and diastolic failure
Seen in disease states such as dilated cardiomyopathy (DCM)
Poor EFs (<35%)
High pulmonary pressures
Biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity)

9. Compensatory Mechanisms
Release of catecholamines (epinephrine and norepinephrine)
Increased heart rate (HR)
Increased myocardial contractility
Peripheral vasoconstriction
These increase myocardial oxygen demand and workload
Kidneys release renin
RAAS
Antidiuretic hormone (ADH) is secreted and causes
Increased water reabsorption in the renal tubules leading to water retention and increased blood volume

10. Compensatory Mechanisms
Endothelin is stimulated by ADH, catecholamines, and angiotensin II and causes
Arterial vasoconstriction
Increase in cardiac contractility
Hypertrophy
Proinflammatory cytokines (e.g., tumor necrosis factor)
Released by cardiac myocytes in response to cardiac injury
Depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and myocyte cell death
Over time, a systemic inflammatory response is mounted, resulting in
Cardiac wasting
Muscle myopathy
Fatigue

11. Consequences of compensatory mechanisms
Ventricular dilation: Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated
Initially an adaptive mechanism
Eventually this mechanism becomes inadequate and CO decreases
Hypertrophy: Increase in the muscle mass and cardiac wall thickness
Has poor contractility
Has higher oxygen needs
Has poor coronary artery circulation
Is prone to ventricular dysrhythmias

12. Counterregulatory processes
Natriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP)
Released in response to increases in atrial volume and ventricular pressure
Promote venous and arterial vasodilation, reducing preload and afterload
Prolonged HF leads to a depletion of these factors
Natriuretic peptides are endothelin and aldosterone antagonists
Enhance diuresis
Block effects of the RAAS
Natriuretic peptides inhibit the development of cardiac hypertrophy and may have antiinflammatory effects

13. Counterregulatory processes
Nitric oxide (NO)
Released from the vascular endothelium in response to the compensatory mechanisms
NO relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload

14. Types of Heart Failure
Left-sided HF (most common) from left ventricular dysfunction (e.g., MI hypertension, CAD, cardiomyopathy)
Backup of blood into the left atrium and pulmonary veins
Pulmonary congestion
Edema

15. Left-sided Heart Failure
Fig. 35-1

16. Types of Heart Failure
Right-sided HF from left-sided HF, cor pulmonale, right ventricular MI
Backup of blood into the right atrium and venous systemic circulation
Jugular venous distention
Hepatomegaly, splenomegaly
Ascites
Peripheral edema

17. Clinical Manifestations
Acute decompensated heart failure (ADHF)
Pulmonary edema, often life-threatening
Early
Increase in the respiratory rate
Decrease in PaO2
Later
Tachypnea
Respiratory acidosis

18. Clinical Manifestations (Cont’d)
Acute decompensated heart failure (ADHF)
Physical findings
Orthopnea
Dyspnea, tachypnea
Use of accessory muscles
Cyanosis
Cool and clammy skin

19. Clinical Manifestations (Cont’d)
Acute decompensated heart failure (ADHF)
Physical findings
Cough with frothy, blood-tinged sputum
Breath sounds: Crackles, wheezes, rhonchi
Tachycardia
Hypotension or hypertension

20. Pulmonary Edema
Fig. 35-2

21. Clinical Manifestations
Chronic heart failure
Fatigue
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants

22. Clinical Manifestations (Cont’d)
Dependent edema
Edema may be pitting in nature
Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate an exacerbation of HF
Renal failure may contribute to fluid retention
Nocturia
Skin
Dusky, cool, damp to touch
Lower extremities: Shiny and swollen, diminished or absent hair growth, pigment changes

23. Clinical Manifestations (Cont’d)
Chronic heart failure
Restlessness, confusion, decreased memory
Chest pain (angina)
Anorexia, nausea

24. Atrial fibrillation (most common dysrhythmia)
Complications
Pleural effusion
Atrial fibrillation (most common dysrhythmia)
Loss of the atrial contraction (kick) can reduce CO by up to 30%
Promotes thrombus/embolus formation
Treatment may include cardioversion, antidysrhythmics, and/or anticoagulants
High risk of fatal dysrhythmias with HF and an EF <35%
HF can lead to severe hepatomegaly, especially with RV failure
Fibrosis and cirrhosis can develop over time
Renal insufficiency or failure

25. Diagnostic Studies
Primary goal is to determine underlying cause (work-up will include)
History and physical examination
Chest x-ray
ECG
Lab studies (e.g., cardiac enzymes, BNP)
Hemodynamic assessment
Echocardiogram
Stress testing
Cardiac catheterization
Ejection fraction (EF)

26. Classification Systems
New York Heart Association Functional Classification of HF
Classes I to IV
ACC/AHA Stages of HF
Stages A to D

27. Nursing and Collaborative Management
Overall goals of therapy for ADHF and chronic HF
Decrease patient symptoms
Improve LV function
Reverse ventricular remodeling
Improve quality of life
Decrease mortality and morbidity

28. Nursing and Collaborative Management ADHF
Decrease intravascular volume
Reduces venous return and preload
Loop diuretics (e.g., furosemide)
Ultrafiltration or aquapheresis
Decrease venous return (preload)
Reduces the amount of volume returned to the LV during diastole
High-Fowler’s position
IV nitroglycerin

29. Nursing and Collaborative Management ADHF (Cont’d)
Decrease afterload
Improves CO and decreases pulmonary congestion
IV sodium nitroprusside (Nipride)
Morphine sulfate
Nesiritide (Natrecor)
Improve gas exchange and oxygenation
Supplemental oxygen
Noninvasive ventilatory support (BiPAP)

30. Nursing and Collaborative Management ADHF (Cont’d)
Improve cardiac function
For patients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine sulfate)
Inotropic therapy
Digitalis
-Adrenergic agonists (e.g., dopamine)
Phosphodiesterase inhibitors (e.g., milrinone)
Hemodynamic monitoring

31. Nursing and Collaborative Management ADHF (Cont’d)
Reduce anxiety
Distraction, imagery
Sedative medications (e.g., morphine sulfate, benzodiazepines)

32. Collaborative Management Chronic HF
Main treatment goals
Treat the underlying cause and contributing factors
Maximize CO
Provide treatment to alleviate symptoms
Improve ventricular function
Improve quality of life
Preserve target organ function
Improve mortality and morbidity

33. Collaborative Management Chronic HF (Cont’d)
Oxygen administration
Physical and emotional rest
Nonpharmacologic therapies
Cardiac resynchronization therapy (CRT) or biventricular pacing
Cardiac transplantation

34. Collaborative Management Chronic HF (Cont’d)
Nonpharmacologic therapies (cont’d)
Intraaortic balloon pump (IABP) therapy
Ventricular assist devices (VADs)
Destination therapy—permanent, implantable VAD

35. Collaborative Management Chronic HF (Cont’d)
Therapeutic objectives for drug therapy
Identification of type of HF and causes
Correction of sodium and water retention and volume overload
Reduction of cardiac workload
Improvement of myocardial contractility
Control of precipitating and complicating factors

36. Collaborative Management Chronic HF (Cont’d)
Drug therapy
Diuretics
Thiazide
Loop
Spironolactone

37. Collaborative Management Chronic HF (Cont’d)
Drug therapy (cont’d)
Vasodilators
ACE inhibitors
Angiotensin II receptor blockers
Nitrates
-Adrenergic blockers
Nesiritide

38. Collaborative Management Chronic HF (Cont’d)
Drug therapy (cont’d)
Positive inotropic agents
Digitalis
Calcium sensitizers
BiDil (combination drug containing isosorbide dinitrate and hydralazine) approved only for the treatment of HF in African Americans

39. Collaborative Management Chronic HF (Cont’d)
Nutritional therapy
Diet and weight reduction recommendations must be individualized and culturally sensitive
Dietary Approaches to Stop Hypertension (DASH) diet is recommended
Sodium is usually restricted to 2.5 g per day

40. Collaborative Management Chronic HF (Cont’d)
Nutritional therapy
Fluid restriction not generally required
Daily weights are important
Same time, same clothing each day
Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to health care provider

41. Nursing Management Chronic HF
Assessment
Subjective Data
Past health history
Functional health patterns
Medications
Objective Data
Physical examination

42. Nursing Management Chronic HF (Cont’d)
Nursing Diagnoses
Activity intolerance
Fluid volume excess
Impaired gas exchange
Anxiety
Deficient knowledge

43. Nursing Management Chronic HF (Cont’d)
Planning: Overall Goals
Decrease in symptoms (e.g., shortness of breath, fatigue)
Decrease in peripheral edema
Increase in exercise tolerance
Compliance with the medical regimen
No complications related to HF

44. Nursing Management Chronic HF (Cont’d)
Health Promotion
Treatment or control of underlying heart disease key to preventing HF and episodes of ADHF (e.g., valve replacement, control of hypertension)
Antidysrhythmic agents or pacemakers for patients with serious dysrhythmias or conduction disturbances
Flu and pneumonia vaccinations

45. Nursing Management Chronic HF (Cont’d)
Health Promotion
Patient teaching: medications, diet, and exercise regimens
Exercise training (e.g., cardiac rehabilitation) improves symptoms but often underprescribed
Home nursing care for follow-up and to monitor patient’s response to treatment may be required

46. Nursing Management Chronic HF (Cont’d)
Acute Intervention
HF is a progressive disease; treatment plans are established with quality-of-life goals
Symptom management is controlled with self-management tools (e.g., daily weights)

47. Nursing Management Chronic HF (Cont’d)
Acute Intervention
Salt must be restricted
Energy must be conserved
Support systems are essential to the success of the entire treatment plan

48. Nursing Management Chronic HF (Cont’d)
Ambulatory and Home Care
Explain physiologic changes that have occurred to patient
Assist patient to adapt to both the physiologic and psychologic changes
Integrate patient and patient’s family or support system in the overall care plan

49. Nursing Management Chronic HF (Cont’d)
Implementation: Patient education
Medications (lifelong)
Taking pulse rate
Know when drugs (e.g., digitalis, -adrenergic blockers) should be withheld and reported to health care provider

50. Nursing Management Chronic HF (Cont’d)
Implementation: Patient Education
Home BP monitoring
Signs of hypo- and hyperkalemia if taking diuretics that deplete or spare potassium
Instruct patient in energy-conserving and energy-efficient behaviors

51. Nursing Management Chronic HF (Cont’d)
Evaluation
Respiratory status
Fluid balance
Activity tolerance
Anxiety control
Knowledge of disease process