Heart Failure - BMH/Tele


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Heart Failure - BMH/Tele

  1. 1. The Vicious Cycle of Heart Failure Natalie Bermudez, RN, BSN, MS Telemetry Course Clinical Educator for Telemetry
  2. 2. Heart Failure <ul><li>Congestive heart failure is the only cardiovascular disorder with increasing incidence and mortality. </li></ul><ul><li>Hospital admissions are rapidly increasing, and has a major impact on quality of life and financial resources. </li></ul><ul><li>In fact, advanced heart failure has become the most costly medical syndrome. </li></ul><ul><li>(Vavouranakis et al, 2003, p. 105) </li></ul>
  3. 3. Statistics <ul><li>According to Chojnowski (2008), “hospital discharges for the diagnosis of heart failure increased a whopping 175% between 1979 and 2004, with 30% to 60% of patients being readmitted within 6 months” (p. 50). </li></ul><ul><li>“ Heart failure accounts for nearly 1 million hospitalizations each year” </li></ul><ul><li>(Moser & Riegel, 2008, p. 916). </li></ul>
  4. 4. More Statistics <ul><li>According to the AHA: </li></ul><ul><li>More than 5 million adults in the U.S. had a HF diagnosis in 2004 </li></ul><ul><li>(Chojnowski, 2007, p. 50) </li></ul><ul><li>While deaths overall decreased 2% between 1994 and 2004, deaths from HF increased 28% </li></ul><ul><li>(Chojnowski, 2007, p. 50) </li></ul><ul><li>According to the American Heart Association’s publication, Heart Disease and Stroke Statistics: 2008 Update At-A-Glance, the estimated indirect and direct cost of hospitalization for acute decompensated heart failure (ADHF) in the United States is $34.8 billion. (expected cost for 2007 was $33.2 billion) </li></ul>
  5. 5. More Statistics <ul><li>On a yearly basis, 12 to 15 million office visits and 6.5 million hospital visits are due to HF </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007) </li></ul><ul><li>“ Despite aggressive investigation into treatment options, until very recently the 5-year mortality rate was 50%” </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1009) </li></ul>
  6. 6. Readmissions <ul><li>As many as 50% of patients with ADHF are readmitted within 6 months of discharge” (Moser & Riegel, 2008). </li></ul><ul><li>Nonadherence to medications or diet </li></ul><ul><li>Failure to seek medical care when symptoms arise </li></ul><ul><li>Receiving inappropriate therapy </li></ul><ul><li>Decreased length of stay </li></ul><ul><ul><li>Premature discharge before all medical issues have been addressed; not meeting D/C criteria </li></ul></ul><ul><li>Inadequate patient education (NB) </li></ul>
  7. 7. What Is HF? <ul><li>HF is the inability of the heart to maintain adequate cardiac output to meet metabolic demands of the body </li></ul><ul><li>More commonly occurs in the left ventricle </li></ul><ul><li>But also happens on the right, but is usually preceded by left-sided heart failure </li></ul>
  8. 8. HF’s Main Issue <ul><li>Leads to fluid overload and inadequate tissue perfusion!!! </li></ul>
  9. 9. Heart Failure <ul><li>Acute versus Chronic HF </li></ul><ul><li>Left-sided versus Right-sided </li></ul><ul><li>Systolic versus Diastolic </li></ul>
  10. 10. Heart Failure <ul><li>HF can severely restrict a person’s ability to perform ADL’s </li></ul><ul><li>Affects person’s quality of life </li></ul><ul><li>Prognosis depends on underlying cause and treatment </li></ul>
  11. 11. Heart Failure <ul><li>PATHOPHYSIOLOGY: </li></ul><ul><li>Underlying cause determines whether HF is chronic or acute </li></ul><ul><li>Associated with systolic or diastolic overloading and myocardial weakness </li></ul>
  12. 12. Heart Failure <ul><li>PATHOPHYSIOLOGY: </li></ul><ul><li>As stress on the heart muscle reaches a critical level, the muscle’s contractility decreases (Frank-Starling) and CO ↓ </li></ul><ul><li>Venous input to the ventricles does not change! </li></ul>
  13. 13. Systolic Heart Failure <ul><li>Pathophysiology </li></ul><ul><li>Results in decreased blood volume ejected from the ventricle </li></ul><ul><li>SNS stimulated & releases epinephrine & norepinephrine -> ↑ HR to maintain CO </li></ul>
  14. 14. Pathophysiology <ul><li>Negative Effects of SNS Stimulation: </li></ul><ul><li>Angiotensin-converting enzyme (vasodilator) is activated in pulmonary vessels -> ↑ B/P and afterload </li></ul><ul><li>Angiotensin II -> aldosterone released -> Na & Fluid Retention -> Stimulates thirst center </li></ul>
  15. 15. Pathophysiology <ul><li>Negative Effects of SNS stimulation: </li></ul><ul><li>What is the end result of this??? </li></ul><ul><li>FLUID VOLUME OVERLOAD!!! </li></ul><ul><li>Causes ↑ workload of the heart! </li></ul>
  16. 16. Pathophysiology <ul><li>Counterregulatory Effects: </li></ul><ul><li>Release of natriuretic peptides, prostaglandins, and nitric oxide </li></ul><ul><li>Natriuretic Peptides: </li></ul><ul><li>ANP (found mainly in the atria) </li></ul><ul><li>BNP (found mainly in the ventricles) </li></ul>
  17. 17. Pathophysiology <ul><li>Counterregulatory Effects: </li></ul><ul><li>Brain Natriuretic Peptide </li></ul><ul><li>Secreted by the ventricles with ventricular volume expansion and pressure overload </li></ul>
  18. 18. Pathophysiology <ul><li>Effects of BNP: </li></ul><ul><li>They are released from the overdistended cardiac chambers </li></ul><ul><li>They promote vasodilation and natriuresis </li></ul><ul><li>When released they also inhibit renin and aldosterone release </li></ul>
  19. 19. Pathophysiology <ul><li>Counterregulatory Effects versus Negative Effects of SNS stimulation: </li></ul><ul><li>This effect is not strong enough to overcome the negative effects of the other mechanisms </li></ul>
  20. 20. Pathophysiology <ul><li>In the End, there is still… </li></ul><ul><li>↑ Workload -> ↓ myocardial contractility -> Increased afterload ventricular dilation -> Increasing workload -> leads to ventricular hypertrophy </li></ul>
  21. 21. Vicious Cycle of HF <ul><li>The heart does not pump sufficient blood to </li></ul><ul><li>body, which causes the body to stimulate </li></ul><ul><li>the heart to work harder; the heart cannot </li></ul><ul><li>respond (due to myocardial damage) and, in spite of counterregulatory mechanisms, </li></ul><ul><li>the failure becomes worse. </li></ul>
  22. 22. Diastolic Heart Failure <ul><li>Develops because of continued increased workload, which responds by increasing the number and size of myocardial cells (i.e., ventricular hypertrophy and altered cell functioning). </li></ul><ul><li>This causes decreased ventricular filling and decreased CO stimulating the SNS in the same fashion as systolic HF. </li></ul>
  23. 23. Etiology <ul><li>Coronary Artery Disease </li></ul><ul><li>Myocardial Infarction </li></ul><ul><li>Hypertension (S or P) </li></ul><ul><li>Rheumatic HD </li></ul><ul><li>Connective Tissue Disease </li></ul><ul><li>Congenital HD </li></ul><ul><li>Thyroid Abnormalities </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Valvular Diseases </li></ul><ul><li>Persistent Tachydysrhythmias </li></ul><ul><li>Toxins (chemo) </li></ul><ul><li>ETOH Abuse </li></ul>
  24. 24. Etiology <ul><li>The chief contributors to the development of HF are coronary artery disease and hypertension, both of which are found in 40% of patients with HF” (Moser & Riegel, 2008, p. 916). </li></ul><ul><li>Regardless of the cause of HF, it is a chronic condition that becomes progressively worse, culminating in the patient’s premature death (Moser & Riegel, 2008, p. 916). </li></ul>
  25. 25. Signs & Symptoms <ul><li>Dyspnea on Exertion </li></ul><ul><li>Orthopnea </li></ul><ul><li>Tachypnea </li></ul><ul><li>Paroxysmal Nocturnal Dyspnea </li></ul><ul><li>Crackles (bases) </li></ul><ul><li>Dullness (percussion) </li></ul><ul><li>Tactile Fremitus </li></ul><ul><li>Displaced Apical Heartbeat </li></ul><ul><li>Tachycardia </li></ul><ul><li>Confusion </li></ul><ul><li>Anxiety/Restlessness </li></ul><ul><li>Impaired Memory </li></ul><ul><li>Diaphoresis </li></ul><ul><li>Cool extremities </li></ul><ul><li>Oliguria </li></ul>Left-Sided HF
  26. 26. Signs & Symptoms <ul><li>Fatigue </li></ul><ul><li>Ascites </li></ul><ul><li>Enlarged Spleen </li></ul><ul><li>Enlarged Liver </li></ul><ul><li>JVD </li></ul><ul><li>Anorexia </li></ul><ul><li>Edema Hands & Finger </li></ul><ul><li>Dependent Edema </li></ul><ul><li>Increased peripheral venous pressure </li></ul>Right-Sided HF
  27. 27. Diagnostic Evaluation <ul><li>ECHO -> determines EF % </li></ul><ul><li>Chest X-ray -> fluid in pulmonary space & possible underlying cause </li></ul><ul><li>EKG -> determine underlying cause </li></ul><ul><li>BUN/Creatinine -> assess for renal failure </li></ul><ul><li>BNP -> high levels indicate CHF (> 100) </li></ul><ul><li>Electrolytes & CBC </li></ul>
  28. 28. 4 Stages of HF <ul><li>Stage A </li></ul><ul><li>Patients at risk for developing heart failure are addressed almost exclusively in the ACC/AHA guidelines </li></ul><ul><li>First-line treatment is lifestyle modifications and drug therapy with ACE inhibitors </li></ul>
  29. 29. 4 Stages of HF <ul><li>Stage B </li></ul><ul><li>Patients with left ventricular dysfunction who have not developed symptoms </li></ul><ul><li>Treatment includes lifestyle modifications and drug therapy with ACE inhibitors, BB’s, and/or cardiac glycosides (for patients with a-fib only) </li></ul>
  30. 30. 4 Stages of HF <ul><li>Stage C </li></ul><ul><li>Patients with left ventricular dysfunction with current symptoms or prior symptoms of heart failure </li></ul><ul><li>Treatment includes lifestyle modifications and drug therapy with ACEIs or ARBs, BB’s, cardiac glycosides, and a diuretic </li></ul>
  31. 31. 4 Stages of HF <ul><li>Stage D </li></ul><ul><li>Patients with refractory end-stage heart failure </li></ul><ul><li>Treatment is usually prescribed by a specialist </li></ul>
  32. 32. Acute HF Exacerbation <ul><li>Supplemental Oxygen Therapy & Diuretics for </li></ul><ul><li>Acute Decompensated HF </li></ul>SYMPTOMATIC TREATMENT
  33. 33. Anticoagulants <ul><li>Used for patients with HF who also have chronic atrial fibrillation </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1012) </li></ul>
  34. 34. Pharmacologic Management <ul><li>PO/IV Medications: </li></ul><ul><li>ACE inhibitors (Vasotec) </li></ul><ul><li>Angiotensin II Receptor Blockers (ARBs) (Diovan) </li></ul><ul><li>Vasodilators (nitroglycerin, nesiritide, nitroprusside) </li></ul><ul><li>Beta-blockers (Coreg, Lopressor, Toprol) </li></ul><ul><li>Diuretics (Lasix, Aldactone, HCTZ, Zaroxolyn) </li></ul><ul><li>Digitalis (digoxin – Lanoxin) </li></ul><ul><li>Calcium channel blockers (Norvasc, Plendil) </li></ul><ul><li>Anticoagulants and Antiplatelets </li></ul><ul><li>Inotropics (dobutamine, dopamine, milrinone) </li></ul><ul><li>Aldosterone Antagonists </li></ul>
  35. 35. ACEIs & ARBs <ul><li>Act on the R-A-A system to decrease preload and afterload </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1012) </li></ul>
  36. 36. ACEIs & ARBs <ul><li>ACEIs are the drug of choice in the treatment of HF (prevents HF exacerbation) </li></ul><ul><li>ACEIs affect both preload and afterload through vasodilatory effects, decrease the incidence of remodeling by reducing the local generation and action of angiotensin II in the heart muscle, and prevent neurohormonal counterregulatory mechanisms that worsen heart failure through their action on the R-A-A system </li></ul><ul><li>( Wynne, Woo, & Olyaei, 2007, p. 1014) </li></ul>
  37. 37. ACEIs & ARBs <ul><li>As monotherapy or in combination with other drugs, ACEIs are superior to all other drugs and drug combinations used to treat HF </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1014) </li></ul>
  38. 38. ACEIs & ARBs <ul><li>Losartan (Cozaar) is officially the only ARB approved for treatment of HF. </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1015) </li></ul>
  39. 39. Beat-Adrenergic Blockers <ul><li>Affect the SNS counterregulatory mechanism of HF </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1012) </li></ul>
  40. 40. Pharmacologic Management <ul><li>WARNING: </li></ul><ul><li>Beta-Blocker therapy with diastolic HF may cause exacerbation of symptoms </li></ul><ul><li>Negative Inotropic & Chronotropic Effects </li></ul><ul><li>Decreases heart rate </li></ul><ul><li>Decreases contractility </li></ul>
  41. 41. Vasodilators/Nitrates <ul><li>Improve systolic and diastolic ventricular function by improving oxygen transport to the myocardium for patients with HF who also have angina </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1012) </li></ul>
  42. 42. Antiplatelets <ul><li>Used to prevent myocardial infarction and death in patients with HF who have underlying CAD </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1012) </li></ul>
  43. 43. Pharmacologic Management <ul><li>IV Infusions : </li></ul><ul><li>Natrecor drip (nesitiride) – elevated BNP levels; BP monitored closely </li></ul><ul><li>Primacor drip (milrinone) – promotes vasodilation; BP monitored closely </li></ul><ul><li>Dobutrex drip (dobutamine) – increases cardiac contractility (may cause tachydysrhythmias) </li></ul>
  44. 44. Lanoxin (digoxin) <ul><li>Positive Inotropic Effects: </li></ul><ul><li>Improves cardiac contractility </li></ul><ul><li>Negative Chronotropic Effects: </li></ul><ul><li>Decreases heart rate </li></ul><ul><li>Main uses are with CHF and supraventricular tachycardias </li></ul>Cardiac Glycoside
  45. 45. Lanoxin (digoxin) <ul><li>May be administered PO or IV </li></ul><ul><li>Caution: If given IVP, need to administer slowly over 5 minutes (at least) </li></ul><ul><li>Inform monitor technician prior to administration </li></ul>
  46. 46. Lanoxin (digoxin) <ul><li>ATTENTION!!! </li></ul><ul><li>For severe digoxin toxicity, administer… </li></ul><ul><li>Digibind (Digoxin Immune FAB) </li></ul><ul><li>380 – 760 mg IV </li></ul>
  47. 47. Lanoxin (digoxin) <ul><li>Take apical pulse for 1 full minute prior to administration </li></ul><ul><li>If less than 60, hold and notify physician </li></ul><ul><li>Monitor digoxin levels to evaluate potential toxicity </li></ul><ul><li>S/S – “Yellow Lights” </li></ul>
  48. 48. Lasix (furosemide) <ul><li>Inhibits reabsorption of Na & Cl @ proximal and distal tubule and in the loop of Henle </li></ul><ul><li>Main uses are with CHF, pulmonary edema, and Hypertension </li></ul>Loop Diuretic
  49. 49. Lasix (furosemide) <ul><li>May be administered PO or IV </li></ul><ul><li>Caution: If given IVP, need to administer slowly 20 mg/min </li></ul>
  50. 50. Lasix (furosemide) <ul><li>Monitor B/P prior to and following administration </li></ul><ul><li>Monitor urine output, edema, and lung sounds </li></ul><ul><li>Monitor serum electrolytes (K, Na) </li></ul>
  51. 51. Natrecor (nesiritide) <ul><li>Human BNP bonds to the receptor on vascular smooth muscle and endothelial cells </li></ul><ul><li>Newer medication – use has not become widespread yet… </li></ul>Vasodilator – Human BNP
  52. 52. Therapeutic Interventions <ul><li>Intraaortic Balloon Pump (IABP) </li></ul><ul><li>Most widely used mechanical support device </li></ul><ul><li>Increases blood flow to heart muscle, decreases the workload of the heart, and may be used in the presence cardiogenic shock and ADHF caused by MI </li></ul><ul><li>(Moser & Reigel, 2008, p. 925) </li></ul>
  53. 53. Therapeutic Interventions <ul><li>Intraaortic Balloon Pump (IABP) </li></ul><ul><li>It is placed proximal to the aorta and inflates when the heart relaxes </li></ul><ul><li>This forces the blood forward to perfuse the periphery and backward to fill the coronary arteries </li></ul><ul><li>(Moser & Reigel, 2008, p. 925) </li></ul>
  54. 54. Therapeutic Interventions <ul><li>Left Ventricular Assistive Device (LVAD) </li></ul><ul><li>Used to control acute reversible HF resulting in cardiogenic shock, which is often caused by AMI </li></ul><ul><li>Mechanical support may augment the patient’s circulation until myocardium improves enough for patient to undergo revascularization </li></ul><ul><li>(Moser & Reigel, 2008, p. 925) </li></ul>
  55. 55. DIETARY MANAGEMENT <ul><li>Restrictions </li></ul><ul><li>Low sodium diet </li></ul><ul><li>(2 – 3 grams/day) </li></ul><ul><li>Limited fluid intake </li></ul>
  56. 56. Nursing Interventions & Considerations <ul><li>Monitoring </li></ul><ul><li>Physical Assessment </li></ul><ul><li>Inspection, Auscultation, Palpation </li></ul><ul><li>Lab Values </li></ul><ul><li>Na + , K + , BNP, BUN/creatinine </li></ul><ul><li>Intake and Output </li></ul><ul><li>Fluid & Sodium Restriction </li></ul><ul><li>Urine Output & Daily Weights </li></ul>
  57. 57. Heart Failure <ul><li>Teaching </li></ul><ul><li>Diet Modifications </li></ul><ul><li>Restricted Sodium Intake </li></ul><ul><li>Normal Fluid Intake (after stabilized) </li></ul><ul><li>Medication Regimen </li></ul><ul><li>Common Side Effects </li></ul><ul><li>Adhering to Regimen </li></ul><ul><li>Signs and Symptoms of HF </li></ul><ul><li>Monitor Daily Weights </li></ul><ul><li>Edema </li></ul><ul><li>Shortness of Breath </li></ul>Nursing Interventions & Considerations
  58. 58. Heart Failure <ul><li>“ Because multidrug regimens are often necessary, patient education is essential to limit complications and hospitalizations that result from poor adherence to the treatment regimen” </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1009) </li></ul>Nursing Interventions & Considerations
  59. 59. TJC Core Measures <ul><li>The Joint Commission defines Core Measures as standardized performance measures, with precisely defined data elements, calculation algorithms, and standardized data-collection protocols. In other words, using Core Measures is a way to find out if patients are getting good care. By requiring all organizations to use the same measures, TJC is leveling the playing field so hospitals and clinicians have reliable data for self-assessment, as well as benchmarks for comparisons. </li></ul>
  60. 60. TJC Core Measures <ul><li>Acute Myocardial Infarction </li></ul><ul><li>(AMI) </li></ul><ul><li>Community Acquired Pneumonia </li></ul><ul><li>(CAP) </li></ul><ul><li>Surgical Care Improvement Plan </li></ul><ul><li>(SCIP) </li></ul><ul><li>Heart Failure </li></ul><ul><li>(HF) </li></ul>
  61. 61. TJC Core Measures <ul><li>LVF Assessment (echocardiogram) </li></ul><ul><li>ACEI or ARB for LVSD (EF < 40%) </li></ul><ul><li>Adult smoking cessation advice/counseling </li></ul><ul><li>Discharge instructions include reconciliation of medication regimen </li></ul>Heart Failure
  62. 62. References <ul><li>Chojnowski, D. (2007). Protecting our patients from harm: Taking an aim at heart failure. Nursing 2007, 37 (11), 50-55. </li></ul><ul><li>Hodgson, B. B., & Kizior, R. J. (2007). Saunders nursing drug handbook. St. Louis, MS: Saunders Elsevier. </li></ul><ul><li>Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to braunwald’s heart disease. Saunders Elsevier: St. Louis, MO. </li></ul><ul><li>Nolan, M. N. (2004). JCAHO core measures. Hoffman Estates, IL: Nursing Spectrum. </li></ul><ul><li>Skidmore-Roth, L. et al. (2007). Mosby’s nursing drug reference, (20 th ed.). St. Louis, MS: Mosby Elsevier. </li></ul>
  63. 63. References <ul><li>Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11 th ed.). Philadelphia, PA: Lippincott Williams and Wilkins. </li></ul><ul><li>Vavouranakis, I., et al. (2003). Effect of home-based intervention on hospital readmission and quality of life in middle-aged patients with severe congestive heart failure: A 12-month follow up study. European Journal of Cardiovascular Nursing, 2 (2), 105-111. </li></ul><ul><li>Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitioner prescribers, (2 nd ed.). Philadelphia, PA: F. A. Davis Company. </li></ul><ul><li>http://www.pbm.va.gov/monograph/nesiritidemonograph.pdf </li></ul>