CONGESTIVE HEART FAILURE

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ssilvis
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197666
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CONGESTIVE HEART FAILURE
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2013-02-03 16:43:22
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  1. CHF- data
    • -affects 2-3 million people
    • -38,000 deaths/year
    • -mortality 8X normal population
    • -incidence doubles between 45-74 years of age
    • -most common diagnosis in 65 yrs of age, poor prognosis
  2. CHF PATHO-
    • -ventricle of heart unable to deliver adequate quantities of blood to body tissues
    • -decrease of SV and CO
    • -decrease of SV caused by diastolic or systolic dystunction
    • -CAUSES- intrinsic loss of contractility of myocardium, alterations in pulmonary and peripheral circulation, CAD occurs in 2/3 pts, HTN.
  3. CHF- COMPENSATORY MECHANISMS
    • -increased preload
    • -increased afterload (vascular resistance)
    • -ventircular hypertrophy
    • -dilation, activation of sympathetic nervous system
    • -incrased CO
    • -eventually creates further heart pump dysfunction
  4. LEFT SIDED HEART FAILURE-
    • -decreased blood pumped out by LV
    • -increased pressure forces fluid into tissues causing congestion and edema
    • -decreased diffusion of oxygen and CO2 in lung causes dyspnea
    • -resulting in tissue hypoxia and organ dysfunction
  5. S/S OF LEFT SIDED HEART FAILURE-
    -SOB, cough, cardiomegaly
  6. S/S OF RIGHT SIDED HEART FAILURE-
    -Sacral and ankle edema, hepatomegaly, JVD, ascities, splenomegaly
  7. CHF- COMPENSATORY HUMORAL RESPONSES-
    • 1.  decreased tissue perfusion
    • 2.  activates SNS aldosterone and renin-    ngiotensin-system-
    • 3.  both cause vasoconstriction and decreased cardiac output
    • 4.  angiotensin 2
    • 5.  aldosterone and ADH secretion
    • 6.  increased sodium and water retention, increased plasma volume and increased venous pressure.
    • 7.  cardia remodeling, wall thinning
    • 8.  systolic and diastolic dysfunction
    • 9.  decrease in cardiac output and increased circulatory congestion
  8. CHF- UNDERLYING DISORDERS-
    • CARDIAC-
    • 1.  MI
    • 2.  Acute or chronic CAD
    • 3.  Valvular D/O
    • 4.  Arrhythimias
    • 5.  Viral cardiomyopathy

    • NON-CARDIAC-
    • 1.  Severe anemia
    • 2.  Thiamine deficiency
    • 3.  certain anticancer drugs
  9. CHF DIASTOLIC AND SYSTOLIC DYSFUNCTION
    • Diastolic dysfunction- inability of ventricles to properly fill due to increased TPR.
    • Systolic- inability of ventricles to empty
  10. CHF S/S's-
    • 1.  SOB/DOE
    • 2.  exertional
    • 3.  orthopnea
    • 4.  paroxysmal noctural dyspnea
    • 5.  weakness and fatigue
  11. CHF NYS heart association functional classification:
    • Stage 1- no limitation in physical activity
    • 2- slight limitation of physical activity
    • 3- marked limitation
    • 4- severe limitation
  12. CHF GOALS-
    • -treat underlying CHF
    • -factors that produce or worsen HR are identified or minimized
    • -survival becomes important
  13. ACE's-
    • -cornerstone for rx of CHF
    • -decrease preload and afterload
    • -increase cardia index and increase ejection fraction
    • -decrease s/s of CHF
    • -attentuate ventricular dilation and remodeling
    • -improve survival
    • -MOA- inhibit RAAS
    • -block angiotensin 2
    • -produces vasodilation and decrease in TPR
    • -decrease aldosterone and decrease water and na retention
    • -increase serum potassium
    • -VASODILATION- inhibits fluid accumulation, decrease blood flow to vital organs, decrease venous pressure, edema, and increase CO, decrease arterial pressure and cardiac afterload.
    • -INDICATIONS FOR CHF- captopril, lisinopril, ramipril, tranolopril
    • -CONTRAINDICATIONS- angioneurotic edema, auric renal failure.
    • -PRECAUTIONS- hypotension, increased creatinine levels, bilateral renal artery stenosis, hyperkalemia, first dose hypotenstion, dry cough
  14. ANGIOTENSIN 2 TYPE 1 RECEPTOR BLOCKERS-
    • -block effect of angiotensin 2
    • -do not block degradation of vasoactive substances
    • -cozaar, losartan
  15. ACEI AND ARBS-
    -monitor renal function prior to therapy, after one week of therapy, monthly during the first 3 months, when increasing the dose, should be reduced if serum creatinine is more than 2.5.
  16. DIURETICS-
    • -increased sodium and water excretion
    • -decrease preload by decreasing volume overload
    • -titrate dose based on WEIGHT
    • -record DAILY WEIGHTS
    • -INTERACTIONS- NSAIDS and lithium
  17. BB's-
    • -decrease SNS can decelerate progression of HF
    • -SNS increases HR, increases myocardial oxygen demand, cardiac hypertrophy, impaired myocyte function, myocyte death
    • -increase renin which changes angiotensin 1 to 2
    • -used when EF 35-40%- add to existing regimen
    • -CARVEDILOL (ONLY BB APPROVED FOR CHF)
    • -ADVERSE EFFECTS- dizziness, fatigue, worsening HF, bradycardia, hypotenstion, edema, sinusitus
  18. DIGITALIS GLYCOSIDES-
    • -Digoxin and Digibind
    • -absorbed from gut
    • -widley distributed to all tissues including CNS
    • -half life 35 hours
    • -eliminated by kidneys
    • -low rx index
    • -increases parasympathetic tone, decreases sympthatetic tone
    • -positive ionotropic effect which increases force of contraction
    • -decreased chronotropic effect- decreases HR
    • -negative dromotropic effect- decrease in condution velocity
    • -increase in intracellular calcium
    • -increase CO- decrease sypathetic tone
    • -ELECTROPHYSIOLOGY S/E- spontaneous afterdepolarization due to excess calcium in cardiac cells due to higher doses of digoxin- decreased QT interval, increased PR interval, ST segment depression
    • -S/E's- gI, N/V, AV block and tachyarrthmias, blurred vision, yellow/green/blue chromatopsia (hue around objects), gynecomatia, bradycardia
    • -testing dig levels (0.8-2)- READY STATE is acheived in 1-2 weeks so test
    • -INTERACTIONS- decrased absoprtion of digoxin from antacids, cholestyramines, diuretions can cause decreased K.
  19. OTHER DRUGS FOR CHF-
    • -Dobutamine/Dopamine- for acute HF and cardiogenic shock.
    • -Phosphodiesterase inhibitors- amrinone, mirnone- therapy for arrhythmias- short term use.
    • -Phosphodiesterase inhibitors- long-term use for thrombocytopenia, ventricular arrhythmias
  20. VASODILATORS-
    • -hydralazine orminoxidil
    • -decreases resistance the heart encounters during contraction- used in combination with long actingnitrate
    • -S/E- "lupus-like syndrome", tachycardia, edema, hypertrichosis on face, arms, legs and back
  21. VASODILAOR - NITROPURSSIDE-
    • -indications- hypertensive EMERGENCY- acute CHF- and cardiogenic shock
    • -rapid onset of action
    • -BP can be adjusted to practically any level
    • -BP MUST BE CONTINUALLY MONITORED ONCE ABSORBED, BREAKS DOWN TO RELEASE NITRIC OXIDE WHICH ACTIVATES GUANYLATE CYCLASE (SMOOTH MUSCLE ENZYME).
    • -enzyme catalyzes the production of cyclic GMP, which causes vasodilation
    • -can trigger rentention of NA and water (lasix can offset)
    • -WHEN D/C BP RAPIDLY RETURNS TO PRE RX LEVELS
    • -ADVERSE EFFECTS- excessive decrease in BP, cyanide poisioning (rare), thiocyanate toxicity
  22. CHF STEPS IN TREATMENT-
    • 1.  Diuretics
    • 2.  ACE's
    • 3.  digoxin
    • 4.  vasodilators
    • 5.  Angiotnsin 2 inhibitors
  23. ACE'S AND ARB'S CANNOT BE USED IN WHOM?
    -pregnant women

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