Chapter 19

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  1. What is heart failure? Whats the results?
    • inability of heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs
    • -results in congestion of blood flow in systemic/pulmonary venous circulation, inability to ^ cardiac output to meet the demands of activity or ^ tissue metabolism
    • -common in >65 yrs old
  2. What is the etiology and pathogenesis of HF?
    • potential consequence of most cardiac disorders 
    • -commong cause: myocardial ischemia, followed by hypertension and dilated cardiomyopathy
    • -results from impaired ability of myocardial fibers to contract, relax, or both
  3. What is systolic dysfunction?
    • Common etiology: MI - Myocardial infarction 
    • -reduced contractility evidenced by low ejection fraction and reduced inotropy (decreased sympathetic 'tone') during ventricular systole 
    • -impaired contractility involves loss of cardiac muscle cells, β-receptor down regulation, and reduced ATP production
  4. What is diastolic dysfunction?
    • ischemic heart disease and hypertension - main causes 
    • -disorder of myocardial relaxation such that ventricle is excessively noncompliant and does not fill effectively 
    • -low cardiac output, congestion, edema formation with normal ejection fraction
  5. What are the compensatory responses that are currently being reduced to management of HF
    • -SNS activation 
    • -increase preload
    • -myocardial hypertrophy
  6. What is SNS activation?
    • primarily a result of baroreceptor reflex stimulation
    • -CNS ^ activity in sympathetic nerves to the heart resulting in venoconstriction 
    • -juxtaglomerular cells release renin, activating RAAS cascade, resulting in ^ sodium and water retention
  7. What does an increased preload mean?
    • initially a consequence of reduced Ejection Fraction (EF) with resultant ^ in resident end-systolic volume (ESV)
    • -decreased CO to kidney reduces glomerular filtration =fluid conservation 
    • -RAAS cascade activated = elevated blood vol. 
    • Frank-Starling mechanism
  8. What is myocardial hypertrophy; what remodels it?
    • results from chronic elevation of myocardial wall tension (law of Laplace)
    • -high systolic pressure in ventricle needed to overcome a high afterload leading to hypertrophy
    • -neurohormonal factors have hypertrophic effect on heart 
    • -angiotensin II involved in remodeling
  9. What are the clinical manifestations of HF?
    • L ventricular failure - most common
    • -often leads to R ventricular failure
    • -forward failure
    • -backward failure
  10. What is forward failure?
    insufficient cardiac pumping manifested by poor CO
  11. What is backward failure
    congestion of blood behind the pumping chamber
  12. What is L sided HF associated with?
    • backward effects: results in accumulation of blood within pulmonary circulation, pulmonary congestion, and edema 
    • -forward effects: results in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs
  13. What is R-sided HF
    • pulmonary disorders - ^ pulmonary vascular resistance - high afterload - R ventricular hypertrophy - R ventricular failure 
    • -backward effects due to congestion in the systemic venous system 
    • -forward effects cause low output to L ventricle leading to low CO
  14. What are the backward effects of L sided HF?
    • dyspnea on exertion 
    • orthopnea
    • cough
    • paroxygsmal nocturnal dyspnea
    • cyanosis
    • basilar crackles
  15. What are the forward effects of L sided HF
    • fatigue
    • oliguria
    • ^ heart rate
    • faint pulses 
    • restlessness
    • confusion
    • anxiety
  16. What are the forward effects of R sided HF
    • fatigue 
    • oliguria
    • ^ heart rate 
    • faint pulses 
    • restlessness 
    • confusion
    • anxiety
  17. What are the backward effects of R-sided HF
    • hepatomegaly 
    • ascites 
    • splenomegaly
    • anorexia
    • subcutaneous edema
    • jugular vein distention
  18. What is a biventricular HF
    • result of primary L sided HF progressing to R sided HF 
    • -reduced CO 
    • -pulmonary congestion due to L sided HF 
    • -systemic venous congestion due to R sided HF
  19. What are the class and stage of HF? how is it assess?
    • FACES
    • Fatigue
    • Activity limitation
    • Congestion
    • Edema
    • Shortness of breath

    • -assess by xray and echocardiography
    • B type natriuretic peptide lvl 
    • -severity of symptoms used to ID class/stage of HF
  20. treatment of HF
    • improve CO while minimize congestive symptoms and cardiac workload 
    • -by manipulating preload, afterload, and contractility
Card Set:
Chapter 19
2015-02-18 22:42:20
heartfailure dysrhythamias
common sequelae of cardiac disease
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