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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
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
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
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
What are the compensatory responses that are currently being reduced to management of HF
- -SNS activation
- -increase preload
- -myocardial hypertrophy
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
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
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
What are the clinical manifestations of HF?
- L ventricular failure - most common
- -often leads to R ventricular failure
- -forward failure
- -backward failure
What is forward failure?
insufficient cardiac pumping manifested by poor CO
What is backward failure
congestion of blood behind the pumping chamber
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
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
What are the backward effects of L sided HF?
- dyspnea on exertion
- paroxygsmal nocturnal dyspnea
- basilar crackles
What are the forward effects of L sided HF
- ^ heart rate
- faint pulses
What are the forward effects of R sided HF
- ^ heart rate
- faint pulses
What are the backward effects of R-sided HF
- subcutaneous edema
- jugular vein distention
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
What are the class and stage of HF? how is it assess?
- Activity limitation
- Shortness of breath
- -assess by xray and echocardiography
- B type natriuretic peptide lvl
- -severity of symptoms used to ID class/stage of HF
treatment of HF
- improve CO while minimize congestive symptoms and cardiac workload
- -by manipulating preload, afterload, and contractility
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