CONGESTIVE HEART FAILURE

• -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

• -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.

• -increased preload
• -increased afterload (vascular resistance)
• -ventircular hypertrophy
• -dilation, activation of sympathetic nervous system
• -incrased CO
• -eventually creates further heart pump dysfunction

• -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

-SOB, cough, cardiomegaly

-Sacral and ankle edema, hepatomegaly, JVD, ascities, splenomegaly

• 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

• 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

• Diastolic dysfunction- inability of ventricles to properly fill due to increased TPR.
• Systolic- inability of ventricles to empty

• 1.  SOB/DOE
• 2.  exertional
• 3.  orthopnea
• 4.  paroxysmal noctural dyspnea
• 5.  weakness and fatigue

• Stage 1- no limitation in physical activity
• 2- slight limitation of physical activity
• 3- marked limitation
• 4- severe limitation

• -treat underlying CHF
• -factors that produce or worsen HR are identified or minimized
• -survival becomes important

• -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

• -block effect of angiotensin 2
• -do not block degradation of vasoactive substances
• -cozaar, losartan

-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.

• -increased sodium and water excretion
• -decrease preload by decreasing volume overload
• -titrate dose based on WEIGHT
• -record DAILY WEIGHTS
• -INTERACTIONS- NSAIDS and lithium

• -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

• -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.

• -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

• -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

• -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

• 1.  Diuretics
• 2.  ACE's
• 3.  digoxin
• 4.  vasodilators
• 5.  Angiotnsin 2 inhibitors

-pregnant women