1. Interventions for Clients with Cardiac Problems

2. Heart Failure
Also called pump failure, general term for the inadequacy of the heart to pump blood throughout the body; causes insufficient perfusion of body tissue with vital nutrients and oxygen
Left-sided heart failure
Right-sided heart failure
High-output failure

3. Compensatory Mechanisms
Increased heart rate
Because cardiac output is the product of heart rate and stroke volume, an increase in heart rate results in an immediate increase in cardiac output. An increase in heart rate is limited in its ability to compensate for decreased cardiac output. If heart rate becomes too rapid, diastolic filling time is limited and cardiac output may start to fall. An increase in heart rate also significantly increases oxygen demand by the myocardium. If the heart is poorly perfused because of arteriosclerosis, heart failure may worsen
Improved stroke volume
Stroke volume is also improved by sympathetic stimulation. Sympathetic stimulation increases venous return to the heart, which further stretches the myocardial fibers. This increased stretch is referred to as preload. In accordance with Starling's law of the heart, increased myocardial stretch results in more forceful contraction, which increases stroke volume and cardiac output. After a critical point is reached, further volume and stretch reduce the force of contraction and cardiac output

4. Compensatory Mechanisms
Arterial vasoconstriction
Sympathetic stimulation also results in arterial vasoconstriction. Constriction of the arteries has the benefit of maintaining blood pressure and improving tissue perfusion in low-output states. However, constriction of the arteries increases afterload, the resistance against which the heart must pump. Afterload is the major determinant of myocardial oxygen requirements. As afterload increases, the left ventricle requires more energy to eject its contents, and stroke volume may decline
Sodium and water retention
Reduced blood flow to the kidneys, a common occurrence in low-output states, results in the activation of the renin-angiotensin-aldosterone mechanism. Vasoconstriction becomes more pronounced in response to angiotensin, and aldosterone secretion causes sodium and water retention. The volume of blood returning to the left ventricle is further increased by activation of this mechanism

5. Compensatory Mechanisms
Myocardial hypertrophy
Myocardial hypertrophy, with or without chamber dilation, is the final compensatory mechanism. The walls of the heart thicken to provide more muscle mass. This results in more forceful contractions, further increasing cardiac output. However, cardiac muscle may hypertrophy more rapidly than collateral circulation can provide adequate blood supply to the muscle. Often, a hypertrophied heart is slightly oxygen deprived

6. Etiology
Heart failure is caused by systemic hypertension in 75% of cases.
About one third of clients experiencing myocardial infarction also develop heart failure.
Structural heart changes, such as valvular dysfunction, cause pressure or volume overload on the heart.

7. Left-Sided Heart Failure
Manifestations include:
Weakness
Fatigue
Dizziness
Confusion
Pulmonary congestion
Shortness of breath
(Continued)

8. Left-Sided Heart Failure (Continued)
Oliguria
Organ failure, especially renal failure
Death
Assessment
Palpation the precordium - increased heart size is common, with a displacement of the apical impulse to the left.
On auscultation, the nurse may hear a third heart sound (S3) gallop, an early diastolic filling sound indicating an increase in left ventricular pressure. A fourth heart sound (S4) can also occur; it is not a sign of failure but is a reflection of decreased ventricular compliance.
Crackles and wheezes may be present on auscultation of the lungs. Late inspiratory crackles and fine profuse crackles that repeat themselves from breath to breath and do not diminish with coughing indicate heart failure. Crackles usually develop in the bases and spread upward as the condition worsens. Wheezes indicate a narrowing of the bronchial lumen caused by engorged pulmonary vessels

9. Right-Sided Heart Failure
Manifestations include:
Distended neck veins, increased abdominal girth
Hepatomegaly (liver engorgement)
Hepatojugular reflux
Ascites
Dependent edema
Weight: the most reliable indicator of fluid gain or loss

10. Assessments Laboratory assessment Radiographic assessment
Electrocardiography – may demonstrate ventricular hypertrophy, dysrhythmias, and any degree of myocardial ischemia, injury, or infarction
Echocardiography - is useful in diagnosing cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy
Pulmonary artery catheters
S&P

11. Impaired Gas Exchange Interventions include:
Ventilation assistance (promotion of the optimal spontaneous breathing pattern that maximizes oxygen and carbon dioxide exchange in the lungs)
Hemodynamic regulation (optimization of heart rate, preload, afterload, and contractility)
Energy management, diet therapy, drug therapy

12. Decreased Cardiac Output
Interventions include:
Optimization of cardiac output: stroke volume (determined by preload, afterload, and contractility) and heart rate
(Continued)

13. Decreased Cardiac Output (Continued)
Drug therapy including:
Angiotensin-converting enzyme inhibitors ( afterload)
Diuretics ( preload)
Human B-type natriuretic peptides ( afterload)
Nitrates
Inotropics
Beta-adrenergic blockers ( preload)

14. Hemodynamic Regulation
Interventions include:
Reduce afterload.
Reduce preload.
Improve cardiac muscle contractility.
Administer drugs as prescribed.
Monitor for therapeutic and adverse effects.
Teach client and family drug therapy.

15. Drugs That Reduce Afterload
Angiotensin-converting enzyme (ACE) inhibitors
Human B-type natriuretic peptides

16. Interventions That Reduce Preload
Diet therapy
Fluid, sodium restrictions
Drug therapy
Diuretics
Venous vasodilators

17. Drugs That Enhance Contractility
Digitalis
Digitalis toxicity includes anorexia, fatigue, changes in mental status.
Monitor heart rate and electrolytes.
Other inotropic drugs including dobutamine, milrinone, and levosimendan
Beta-adrenergic blockers
S&P

18. Other Nonsurgical Options
Continuous positive airway pressure
Cardiac resynchronization therapy
Investigative gene therapy

19. Surgical Management Newer surgical therapies include the following:
Partial left ventriculectomy
Endoventricular circular patch
Acorn cardiac support device
Myosplint

20. Activity Intolerance Interventions include: Ventilation assistance
Hemodynamic regulation
Energy management
Interdisciplinary interventions, which regulate energy to prevent fatigue and optimize function
Sentence and phrases

21. Potential for Pulmonary Edema
Interventions include:
Assess for early signs, such as crackles in the lung bases, dyspnea at rest, disorientation, and confusion.
Rapid-acting diuretics are prescribed, such as Lasix or Bumex.
Oxygen is always used.
Strictly monitor fluid intake and output.
Sentences and phrase

22. Valvular Heart Disease
Mitral stenosis
Mitral regurgitation (insufficiency)
Mitral valve prolapse
Aortic stenosis
Aortic regurgitation (insufficiency)

24. Assessment
Client may become suddenly ill or slowly develop symptoms over many years.
Question client about attacks of rheumatic fever, infective endocarditis, and possibility of IV drug abuse.
Obtain chest x-ray, echocardiogram, and exercise tolerance test.
Sentences and phrases

25. Common Nursing Diagnoses
Decreased Cardiac Output related to altered stroke volume
Impaired Gas Exchange related to ventilation perfusion imbalance
Activity Intolerance related to inability of the heart to meet metabolic demands during activity
Acute Pain related to physiologic injury agent (hypoxia)

26. Nonsurgical Management
Drug therapy, including diuretics, beta blockers, digoxin, oxygen, and sometimes nitrates
Prophylactic antibiotic
Management of atrial fibrillation, cardioversion
Anticoagulant
Rest with limited activity

27. Surgical Management Reparative procedures Balloon valvuloplasty
Direct, or open, commissurotomy
Mitral valve annuloplasty
Replacement procedures

30. Infective Endocarditis
Microbial infection involving the endocardium
Occurs primarily with IV drug abuse, valvular replacements, systemic infections, or structural cardiac defects
Possible ports of entry: mouth, skin rash, lesion, abscess, infections, surgery, or invasive procedures including IV line placement

31. Manifestations
Clinical manifestations usually occur within 2 weeks of a bacteremia.
Assessment usually reveals a recurrent fever.
Most clients have temperatures from 37.2° to 39.4° C.
Many older adults remain afebrile.
The severity of symptoms may depend on the virulence of the infecting organism

32. Manifestations

33. Manifestations
Fever associated with chills, night sweats, malaise and fatigue
Anorexia and weight loss
Cardiac murmur (newly developed or change in existing)
Development of heart failure
Evidence of systemic embolization
Petechiae
Splinter hemorrhages
Osier's nodes
Janeway's lesions
Splenic infarction
Neurologic changes

34. Janeway's lesions on the sole of the foot
Splinter hemorrhage lesions in endocarditis

35. Interventions Antimicrobials Rest, balanced with activity
Supportive therapy for heart failure
Anticoagulants
Surgical management

36. Pericarditis
Inflammation or alteration of the pericardium, the membranous sac that encloses the heart
Dressler’s syndrome
Postpericardiotomy syndrome
Chronic constrictive pericarditis

37. Assessment
Substernal precordial pain radiating to left side of the neck, shoulder, or back
Grating, oppressive pain, aggravated by breathing, coughing, swallowing
Pain worsened by the supine position; relieved when the client sits up and leans forward
Pericardial friction rub
Sentences and phrases

38. Interventions
Hospitalization for diagnostic evaluation, observation for complications, and symptom relief
Nonsteroidal anti-inflammatory drugs
Corticosteroid therapy
Comfortable position, usually sitting
Pericardial drainage
(Continued)
Sentence and phrases

39. Interventions (Continued)
Chronic pericarditis: radiation or chemotherapy
Uremic pericarditis: dialysis
Pericardiectomy

40. Emergency Care of Cardiac Tamponade
Cardiac tamponade — an extreme emergency
Increased fluid volume
Hemodynamic monitoring
Pericardiocentesis
Pericardial window
Pericardiectomy

41. Rheumatic Carditis
Sensitivity response that develops following an upper respiratory tract infection with group A beta-hemolytic streptococci
Inflammation in all layers of the heart
Impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage

42. Clinical Manifestations
Tachycardia
Cardiomegaly
New or changed murmur
Pericardial friction rub
Precordial pain
Changes in electrocardiogram
Indications of heart failure
Existing streptococcal infection

43. Cardiomyopathy Subacute or chronic disease of cardiac muscle
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy

45. Interventions Nonsurgical management Surgical management
Cardiomyoplasty
Heart transplantation