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22 Cards in this Set
- Front
- Back
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heart failure
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compensated -(adaptive mechanisms can maintain a normal cardiac
output at rest, but the cardiac reserve is very low or absent) uncompensated cardiac output at rest is less than 5 liters per min and is unable to maintain a normal renal function) |
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features of hypertrophy
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- decreasd ca+2 uptake to SR
- capillary network may not increase - pressure overload (concentric hypertrophy) > volume overload (eccentric hyper) |
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circular death in HF
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reduced CO
- SNS + renin activated - vasoconst - increase afterload + work - increased energy - more cellular death - more reduced CO |
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SNS in HF
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- 2x-3x elevation of NE = to LV dysfunction
- down regulation of beta receptors (can be reversed with beta blocker) - increased Gi protein (inhibits a cyclase) |
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Cardiac Glycosides
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DIGOXIN (digitalis)
- steriod nucleus + linked sugars + ring (activity) inhibits Na/K+ pump - increased Na+ concentrations decreased 1ca/3na exchanged - increase IC ca+2 --- increased forced of contraction of the myocardium Also falicitaes ca+ entry through voltage gated ca+ channels increases CONTRACTILITY not contraction...amount of Force w/ same fiber length ~ does not occur in skeletal - occurs in both nml & failing heart - increases 02 consumption in NML heart, reduces in failing heart |
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electrophysio
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theaputic dose: decreased AP duration
toxic: increased slope of phase 4 depolarization increased (less -) maximal diastolic membrane potential - all arrythmic |
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cardicac G - brady effect
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negative chronot effect from
1. vagal activation 2. depressiive action on SA/AV node 3. compenstation of cardiac insuff (most prevalent in failing heart) Vessels - increased vasc tone in art/vens (pts w/ HF...deceased vasc tone...because increased CO offsets VC) 1/2 life 40 HOURS |
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cardiac glycoside - toxic
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narrow TI
- tox dose dept affects heart and CNS 1. CVS - arrhytmias (80%) GI nausea/vomiting (earilest sign) CNS -nightmare, disorentation (digitalis delirium) Visual - green-yellow halos around bright objets, diplopia/amblyopia THERAPY - k+ or mg++ - lidocaine/phentoin for tachy - FAB fragments, DIGIBind..in OD |
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cardiac arryh locations in cardaic Gly
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- ventricular extrasystole (33%
- nonparoxsymal junct tachy 17% - ventricular tachy |
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factors influencing individual sent to cardiac glycosides
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- MI
- electroylte disturbance (hyper/hypo kalemia, hypercalciema, hypomag) - acidicosis (na+/K+ depressed) - renal impairment - hypoxemia (severe pulm disease) - thyroid disease |
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electrolyte disturbances
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- hypercalemia
- hypokalemia - hyperkalemia (bradyarryh) |
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digoxin drug interactions
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Quinidine
Amiodarone Verapamil Cyclosporine - increase serum of digoxin macrolides tetracyclines amnioglycosides - decreased intestitonal biotransformation of digoxin by bacteria of intestinal loop & thiazide - drug induced hypoK and hypoMg |
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contraindications/uses
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diastolic dysfunction (due to ca+ increased..impairs diastolic)
USES HF A-fib, atrial/nodal tachycardia (depressent affects on AV condtion..helps control) |
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b-1 receptor agonists
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contraction/rlx faster & stronger
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dopamine
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activation of D1 - LD
b1/b2, release NE - ID a1 + d2 - HD LD - renal vasodialation ID - + inotropic HD - HR, HTN, N/V ALL Undergo tolerance USE - poor renal perfusion - cardiac failure, shock |
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dobutamine
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b1
- positive inotropic effect (the effect is greater than that of cardiac glycosides and similar to that of milrinone) in HF - lowers LVP (improves cornary perfusion) USE - cardiac failure/shock...when LV is depressed (<2.0 cardiac index) - EMERGENICES ADVERSE - arrhythmias - n/v |
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phosphodiesterase inhibitors
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milrinone
MOA: inhibits phosphodiesterase 3 ~ inactivates cAMP - increase in cAMP a. increases ca+2 IC b. SMC inactivates myosin light chain kinase (decreases phosp of myosin light chain) - + inotropic - perp vasoD....decrease in pulm vasc resistance USE second choice drug when pt is under chronic B blocker Adverse: syncope |
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strategy in CHF
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1. REDUCE WORKLOAD
- vasodilator 2. control of excessive salt & water rentention - low NA diet - mechanical remvoal of fluid 3. improvement of pumpin performance - digitials + inotropic vasodilator therapy in HF - VC due to increases in - SNS - increased catechol - renin - vasopression - thickeness of wall |
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ACE-inhibitors CHF
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coronerstone therapy for all stages
- afterload is reduced (reduction of angiotension levels) - Periferal resistance - reduce aldosterone (preload reduced) - reduces myocardial fibrosis/apoptosis - remodeling, hypertrophy - NE release |
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Atrial natrietric pepetide in acute HF
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- nesitritde (brain nat peptide)
- increased syn of cGMP - art/ven dialation, increased diuresis Adverse Hypotension - RENAL failure acute decompensated HF |
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aldosterone antag - CHF
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spironolactone
- stops pathological remodeling |
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beta blockers CHF
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(Metoprolol)
(Carvedilol) - DANGERous in AHF - good in diastolic cardiac fail..slow cardiac rate/contraction velocity - Chronic systolic failure 1. prevents chronic overactivy of SNS - decreases HR - reduces remodeling 3. upregulation of b1 receptors Recommended in most stages of CHF |
