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HEART FAILURE by Nancy Jenkins

HEART FAILURE by Nancy Jenkins. The most common reason for hospitalization in adults >65 years old. Heart Failure. Cardiogenic shock Cardiomyopathy. Uncompensated Heart Failure Pulmonary Edema-ADHF. Severe End Stage. Mild. Mild. Control With. /Same as Mild with Morphine Sulfate.

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HEART FAILURE by Nancy Jenkins

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  1. HEART FAILUREby Nancy Jenkins • The most common reason for hospitalization in adults >65 years old.

  2. Heart Failure Cardiogenic shock Cardiomyopathy Uncompensated Heart Failure Pulmonary Edema-ADHF Severe End Stage Mild Mild Control With /Same as Mild with Morphine Sulfate Irreversible Needs new ventricle VAD IABP Drugs Diet Fluid Restriction VAD IABP Heart Transplant

  3. Heart Failure Pneumonic U Upright Position N Nitrates L Lasix O Oxygen A Amiodorone, ACE, ARBs D Dig, Dobutamine M Morphine Sulfate E Extremities Up or Down

  4. Definition • CO=SVxHR is insufficient to meet the metabolic needs of the body • SV is determined by preload, afterload and myocardial contractility • Systolic failure- dec. contractility • Diastolic failure- dec. filling • EF< 40%

  5. Heart FailureEtiology and Pathophysiology • 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) http://coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module15/Part02/M15L04S41a.html??hostType=undefined&authorName=Mccance&prodType=undefined

  6. Systolic Failure hypokinesis

  7. 90/140= 64% EF- 55-65 normal

  8. Heart FailureEtiology and Pathophysiology • 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)

  9. Heart FailureEtiology and Pathophysiology • 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)

  10. Preload • Volume of blood in ventricles at end diastole. • Depends on venous return • Depends on compliance

  11. Afterload • Force needed to eject the blood into the circulation • Arterial B/P, pulmonary artery pressure • Valvular disease increases afterload

  12. CHF • Pathophysiology • A. Cardiac compensatory mechanisms • 1.tachycardia • 2.ventricular dilation-Starling’s law • 3.myocardial hypertrophy • Hypoxia leads to dec. contractility http://www.heartsite.CHF/html/chf_3.html

  13. cont. • B.Homeostatic compensatory mechanisms • Sympathetic Nervous System-(beta blockers block this) • 1.vascular system- norepinephrine- vasoconstriction(What effect on afterload?) • 2.kidneys- • A. dec. CO and B/P cause renin angiotensin release.(ACE) • B. Aldosterone release causes Na and H2O retention • Inc. Na causes release of ADH(diuretics) • Release of atrial natriuretic factor- promotes Na and H20 excretion and prevents severe cardiac decompensation • 3.liver- stores venous volume(ascites, +HJR, • Hepatamegaly- can store 10 L. check enzymes

  14. Heart FailureEtiology and Pathophysiology • Compensatory mechanisms are activated to maintain adequate CO • Neurohormonal responses: Endothelin is stimulated by ADH, catecholamines, and angiotensin II and causes • Arterial vasoconstriction • Increase in cardiac contractility • Hypertrophy

  15. Heart FailureEtiology and Pathophysiology • Compensatory mechanisms are activated to maintain adequate CO • Neurohormonal responses: 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

  16. Heart FailureEtiology and Pathophysiology • Compensatory mechanisms are activated to maintain adequate CO • Neurohormonal responses: Over time, a systemic inflammatory response is mounted resulting in • Cardiac wasting • Muscle myopathy • Fatigue

  17. Heart FailureEtiology and Pathophysiology • Counter regulatory 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

  18. Heart FailureEtiology and Pathophysiology • Counter regulatory processes • 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

  19. Result of Compensatory Mechanisms Heart Failure

  20. PathophysiologyStructural Changes • Decreased contractility • Increased preload (volume) • Increased afterload (resistance) • Ventricular remodeling(ACE inhibitors can prevent this) • Ventricular hypertrophy • Ventricular dilation

  21. Heart Failure- Hypertrophy

  22. Ventricular remodeling

  23. END RESULT FLUID OVERLOAD AND EDEMA

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

  25. AHA Newer Classifications of Heart Failure- Staging

  26. Treating the Heart, Blood Vessels and Circulation Stage A • Those at high risk for developing heart failure. Includes people with: • Hypertension • Diabetes mellitus • Coronary artery disease (including heart attack) • History of cardiotoxic drug therapy • History of alcohol abuse • History of rheumatic fever • Family history of CMP • Exercise regularly • Quit smoking • Treat hypertension • Treat lipid disorders • Discourage alcohol or illicit drug use • If previous heart attack or current diabetes mellitus or hypertension ® angiotensin converting enzyme inhibitor (ACE-I) Stage B Those diagnosed with “systolic” heart failure but have never had symptoms of heart failure (usually by finding an ejection fraction of less than 40% on echocardiogram). • Care measures in Stage A + • All patients should be on ACE-I • Beta-blockers should be added • Surgical consultation for coronary artery revascularization and valve repair/replacement (as appropriate) Stage C • Patients with known heart failure with current or prior symptoms. • Symptoms include: • Shortness of breath • Fatigue • Reduced exercise intolerance. • In this group, care measures from Stage A apply, ACE-I and beta-blockers should be used + • Diuretics (water pills) • Digoxin • Dietary sodium (salt) restriction • Weight monitoring • Fluid restriction (as appropriate) • Withdrawal of drugs that worsen the condition • Spironolactone when symptoms remain severe with other therapies ©Cleveland Clinic Foundation Health Information Center, revised 4/02

  27. Treating the Heart, Blood Vessels and Circulation : Usual Therapies Stage D Presence of advanced symptoms, after assuring optimized medical care • All therapies under Stages A, B and C + evaluation for: • Cardiac transplantation • Ventricular assist devices • Surgical options • Research therapies • Continuous intravenous inotropic infusions • End-of-life care

  28. Heart FailureEtiology 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 • Valvular heart disease • Hypervolemia

  29. Classifications • Systolic versus diastolic • Systolic- loss of contractility get dec. CO • Diastolic- decreased filling or preload • Left-sided versus right –sided • Left- lungs • Right-peripheral • High output- hypermetabolic state • Acute versus chronic • Acute- MI • Chronic-cardiomyopathy

  30. Symptoms

  31. Left Ventricular Failure • Signs and symptoms • dyspnea • orthopnea PND • Cheyne Stokes • fatigue • Anxiety • rales • NOTE L FOR LEFT AND L FOR LUNGS

  32. ??????? • WHY DOES THIS OCCUR?

  33. Heart FailureClinical Manifestations • Acute decompensated heart failure (ADHF) • Pulmonary edema, often life-threatening • Early • Increase in the respiratory rate • Decrease in PaO2 • Later • Tachypnea • Respiratory acidemia

  34. Heart FailureClinical Manifestations • Acute decompensated heart failure (ADHF) • Physical findings • Orthopnea • Dyspnea, tachypnea • Use of accessory muscles • Cyanosis • Cool and clammy skin

  35. Heart FailureClinical Manifestations • Acute decompensated heart failure (ADHF) • Physical findings • *Cough with frothy, blood-tinged sputum-why??? • Breath sounds: Crackles, wheezes, rhonchi • Tachycardia • Hypotension or hypertension

  36. Case study of Heart Failure in Lewis online resources

  37. Pulmonary Edema(advanced L side HF) • When PA WEDGE pressure is approx 30mmHg • Signs and symptoms • 1.wheezing • 2.pallor, cyanosis • 3.Inc. HR and BP • 4.s3 gallopThe Auscultation Assistant - Rubs and Gallops • 5.rales,copious pink, frothy sputum

  38. Person literally drowning in secretions Immediate Action Needed

  39. Goals of Treatment • MAD DOG • Improve gas exchange • O2 • intubate • elevate HOB • BIPAP

  40. Right Heart Failure • Signs and Symptoms • fatigue, weakness, lethargy • wt. gain, inc. abd. girth, anorexia,RUQ pain • elevated neck veins • Hepatomegaly +HJR • may not see signs of LVF- why??

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