Heart Failure

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Author:
tiffanydawnn
ID:
134857
Filename:
Heart Failure
Updated:
2012-02-13 00:20:43
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Heart Failure
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Description:
Heart Failure
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  1. heart failure
    • heart is unable to pump sufficient blood to meet metabolic demands of the body
    • decreased cardiac output -> decreased tissue perfusion
    • compensatory mechanisms activated -> vascular congestion
    • develops 2/2 HTN, CAD, COPD
  2. CHF etiology
    • --impaired myocardial contraction r/t damaged muscle s/t MI, inflammation
    • --long standing excessive workload r/t HTN, valve disorders
    • --acute excess demands r/t fluid volume overload, thyroid storm, PE
  3. SNS compensation
    decreased cardiac output -> SNS stimulation -> norepi -> increased HR -> increased CO, vasoconstriction -> increased venous return -> increased ventricular filling/stretch (preload) -> increased contraction -> increased output
  4. RAA compensation
    RAA: decreased cardiac output -> decreased blood flow to kidneys -> renin -> vasoconstriction, aldosterone, ADH -> Na, H20 retention, more vasoconstriction -> increased blood volume -> increased venous return -> increased ventricular filling/stretch (preload) -> increased contraction -> increased output
  5. other compensation
    • atrial/ventricular stretch causes release of ANP/BNP -> excrete Na, H20, inhibit norepi, renin, ADH
    • ventricular remodeling (heart adapts to excess volume) -> ventricular hypertrophy (increased contractility)
  6. CHF decompensation
    • rapid HR -> decreased filling time -> decrease coronary artery perfusion -> increased O2 demand -> ischemia -> impaired output
    • beta receptors less sensitive to continued SNS stimulation -> decreased HR and contractility
    • alpha receptors (peripheral) more sensitive -> increased vasoconstriction -> increased afterload -> increased workload
    • chronic ventricular overfilling -> degenerated ventricle wall -> reduced force of contraction (Frank-Starling fails)
    • chronic distention depletes ANP/BNP -> no inhibition of norepi, renin, ADH -> Na, H20 retention, vasoconstriction -> increased preload and afterload
    • little to no cardiac reserve (ability to quickly adjust to demands)
  7. CHF classifications
    • systolic failure: ventricles fail to contract adequately -> decreased EF -> decreased CO
    • diastolic failure: heart cannot completely relax -> decreased filling -> decreased SV
  8. L-sided failure
    • caused by CAD, HTN
    • can lead to R-sided failure (pulm vascular pressure increases -> R-side workload increases)
    • increased pressure in left chambers -> impaired filling
    • backward -> increased pulmonary congestion -> dyspnea, SOB, cough, orthopnea, cyanosis, crackles, wheezes, S3
    • forward -> decreased cardiac output
  9. R-sided failure
    • caused by L-sided heart failure or acute/chronic pulmonary disease (COPD)
    • increases L-ventricular preload
    • increased pressure in pulmonary vasculature or R ventricle damage -> ineffective pumping
    • backward -> increased systemic congestion -> peripheral edema, anorexia, nausea (GI congestion), enlarged liver, JVD
    • forward -> decreased cardiac output
  10. CHF complications
    • hepatomegaly/splenomegaly r/t engorgement of portal venous system -> increased abd pressure, ascites, GI problems
    • dysrhythmias
    • pleural effusion
    • cardiogenic shock
    • acute pulmonary edema
    • LV thrombus/emboli r/t increased blood stasis s/t decreased EF
  11. CHF dx
    • **ANP/BNP** - hormones released by heart in response to change in blood volume - increased in HF (normal < 100)
    • electrolytes - low serum osmolality r/t fluid retention
    • UA, BUN, creat - kidney function
    • LFTs - monitor liver function
    • thyroid panel - r/o thyroid disorders
    • ABGs - gas exchange (acute HF)
    • CXR - pulmonary vascular congestion, cardiomegaly
    • echo - evaluate structure and function of heart
    • EKG - dysrhythmias, myocardial ischemia and infarction
  12. CHF meds
    • oxygen - pulm congestion
    • **ACE inhibitors**
    • beta blockers
    • diuretics
    • vasodilators
    • positive inotropics
    • anti-dysrhythmics
  13. ACE inhibitors
    • inhibit RAA
    • decreased vasoconstriction, decreased aldosterone
    • decreased cardiac work, increased cardiac output
    • s/e: angioedema, hyperkalemia, cough
  14. beta blockers
    • inhibit SNS (beta 1)
    • can also inhibit beta 2 -> bronchoconstriction
    • use cautiously - reduces force of contraction
  15. diuretics
    • rids excess fluid
    • s/e: electrolyte imbalances
    • loss of vascular volume can stimulate SNS
    • severe HF: Lasix
    • moderate HF: thiazide
  16. vasodilators
    • arterial dilation -> reduces peripheral vascular resistance/afterload
    • venous dilation -> reduces venous return/preload
    • pulmonary dilation -> reduces pressure, allows for reabsorption of extra fluid in lungs
    • nitrates, hydralazine
  17. positive inotropic agents
    • digitalis
    • increases strength of heart contractions by increasing calcium concentration
    • slows conduction through SA node -> increases ventricular filling time
    • monitor dig level - s/s of tox: anorexia, nausea, vomiting, HA, halos
    • low K, low mag, high Ca increase risk of dig tox
  18. antidysrhythmics
    • not usually given d/t depression of left ventricular function
    • amiodarone
  19. diet
    • low sodium - 1.5 - 2 grams daily
    • moderate, progressive exercise program
  20. mechanical assist devices
    • intra-aortic balloon pump
    • left ventricular assist device
  21. CHF surgery
    • cardiomyoplasty - lattimus dorsi used to enhance function of heart
    • cardiac transplant - immunosuppressants, steroids
    • ventricular reduction surgery - removal of part of ventricle to enhance contractility
  22. CHF nursing
    • fluid volume excess
    • activity intolerance
    • impaired gas exchange
    • decreased cardiac output
    • assess for edema, lung sounds, SOB, ascites, nausea
    • O2, rest, daily weight
  23. cardiomyopathy
    • disease of heart muscle
    • affect systolic and diastolic function
    • primary or secondary (ischemia, infection, toxins, tissue disorders, metabolic disorders, nutritional deficiencies)
  24. dilated cardiomyopathy
    • most common (87%)
    • r/t CAD, ETOH, pregnancy
    • dilated heart chambers, impaired ventricular contraction
    • reduced EF (10-20%) -> reduced cardiac output
    • treated like CHF (R and L)
    • 50% mortality/75% after 10 years
    • tx: heart transplant, ACE inhibitors, vasodilators, digoxin
  25. hypertrophic cardiomyopathy
    • decreased chamber size r/t hypertrophy of ventricle
    • decreased ventricular filling -> low cardiac output
    • genetic
    • sudden cardiac death (young athletes) r/t dysrhythmias
    • s/s: dyspnea, angina, syncope, systolic murmur
    • tx: beta blockers, decreased activity, remove muscle, heart transplant
  26. cardiomyopathy dx
    • echo - chamber size and thickness, ventricular wall motion, valve function, systolic/diastolic function
    • EKG - dysrhythmias
    • CXR - size of heart
    • hemodynamics - cardiac output, pressures
    • radionuclear scans - changes in ventricular volume and mass
    • cardiac cath - eval perfusion

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