Heart Failure
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Created by:
rcrhodes1221 on October 10, 2011
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15 terms
Terms | Definitions |
|---|---|
 Normal ejection fraction | - 50% to 70% |
| Primary compensatory mechanisms of heart failure | - the Frank-starling mechanism - Neuroendocrine responses, including activation of the SNS and the renin-angiotensin system - Myocardial hypertrophy |
| Frank-starling mechanism | - the greater the stretch, the greater the force of contraction - increases contractile force => increased Cardiac output - complications: => increased myocardial O2 demand => limited by overstretching |
| Neuroendocrine response | - decreased cardiac output => activate SNS => catecholamine => increase HR, BP and contractility => increased vascular resistance => increased venous return |
| Activation of renin-angiotensin system | - decreased system blood flow is redistributed to the brain and the heart to maintain perfusion => decreased renal perfusion => renin => renin-angiotensin system => vasoconstriction and release aldosterone (from adrenal cortex) and ADH (pituitary gland) |
| Aldosterone | - stimulates Na reabsoprtion & water retention in renal tubules - increases in vascular volume, ventricular filling, force of contraction and improves cardiac output |
| ADH | - inhibit water excretion in distal tubule and vasoconstriction - increases in vascular volume, ventricular filling, force of contraction and improves cardiac output |
| Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) | - counterbalance the effects of renin-angiotensin-aldosterone system and ADH - increased vascular volume and venous return => vasoconstriction, Na and H2O retention => increases the volume and pressures in the heart => stimulate the stretch receptors in the atria and ventricles => release of ANP & BNP (stored in atrial and ventricles) => promote Na and H2O excretion and inhibit the release of NE, renin and ADH => vasodilation => reduces BP - though beneficial but not strong enough to completely compensate heart failure |
| Ventricular remodeling | - fluid volume and pressure increases => heart chambers and myocardium adaptation => chambers dilate to accommodate excess fluid and incomplete emptying => more effective contractions initially => cardiac muscle enlarge increasing its contractile elements and contractility => ventricular hypertrophy - short term regulation of cardiac output but hastens the deterioration of cardiac function |
| Left-sided heart failure | - commonly caused by CAD and HTN - pressure in the pulmonary vascular system increases with congestion behind => right-sided failure - remaining blood in left ventricle => increase pressure in left ventricle and left atrium => impair filling => congestion => increase pressure in pulmonary vascular system => fluid move from blood vessels into interstitial tissues and alveoli => pulmonary congestion (backward effects) and decreased cardiac output (forward effects) |
| Right-sided heart failure | - commonly caused by conditions that restrict blood flow to the lungs, e.g. acute or chronic pulmonary disease - increased pressures in pulmonary vasculature or right ventricular muscle damage => impair the R ventricle's ability to pump blood into the pulmonary circulation => distention of R ventricle and atrium => accumulation of blood in sytemic venous system => increased pressure => congestion of abd organs and peripheral tissue edema |
| Nocturia | - voiding two or more at night - can be developed as edema fluid from dependent tissue is reabsorbed while the client is supine |
| Paroxysmal nocturnal dyspnea | - frightening condition - client awakens at night acutely SOB - occurs when edema fluid that has accumulated during the day is reabsorbed into the circulation at night => fluid overload and pulmonary congestion |
| Cheyne-Stokes respirations | - breathing with rhythmic waxing and waning of depth of breaths - regularly recurring apneic periods |
| Hemodynamic monitoring | - invasive procedure - assess cardiovascular function in the critically-ill clients - evaluate cardiac and circulatory function and the response to interventions |
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