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119 Cards in this Set
- Front
- Back
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What age group is CHF most common in |
>65 |
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what race is it more common in, black or white |
black |
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more common in men or women |
men |
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Even with treatment, 50% of patients with CHF diagnosis die within |
5 years |
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What is the physiological defect of chf |
-reduced contractility -heart is unable to pump sufficient amount of blood to meet the body's demand. |
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what does this lack of O2 supply to meet the body's demand result in |
fatigue oxygen debt acidosis SOB with declining activity |
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causes of CHF |
Myocardial ischemia valvular disease/dysfunction systemic or pulmonary hypertension pericardial disease |
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FUnctional capacity is what |
an assessment of workload -another way to say it is 1 MET is 3.5ml/oxygen/kg/min, normal oxygen consumption at rest |
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poor functional capacity is associated with |
increased cardiac complications in non cardiac surgery |
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how can functional capacity be expressed |
in metabolic equivalents METS |
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one met = |
the oxygen consumption of a 70kg, 40 year old man in a resting state typically 3.5ml/kg/min of O2 |
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What is ventricular failure due to |
systolic dysfunction or diastolic dysfuncton or both |
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systolic dysfunction |
inadequate force generated to eject blood (weak heart) |
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diastolic dysfunction |
reduction in ventricular relaxation interferring with ventricular filling (stiff heart) |
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ventricular remodeling |
can be concentric or eccentric |
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concentric remodeling |
thick wall same chamber size pressure overload systolic problem |
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Eccentric remodeling
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Dilated chamber same wall thickness Diastolic problem |
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Compensatory mechanisms are ________________ nervous system driven |
sympathetic |
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SNS compensatory mechanisms include |
increased preload increased sympathetic tone (HR) activation of RAAS release of ADH ventricular hypertrophy |
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categories of drugs used in CHF |
positive inotropes vasodilators misc drugs for chronic failure |
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positive inotropic drugs |
cardiac glycosides beta agonists PDE inhibitors |
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vasodilators |
PDE inhibitors/milrinone nitroprusside nitrates hydralazine loop diuretics ace inhibs |
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Misc drugs for chronic failures |
loop diuretics ace inhibitors bb's spironolactone thiazides |
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Digitalis is the term used for |
cardiac glycosides |
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they occur naturally |
in plants |
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non glycoside and noncatecholamine drugs used for similar cardiac purpose include |
PDE III inhibitors calcium sensitizers calcium glucagon |
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Dig is derived from what plant |
foxglove |
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basic structure of cardiac glycosides |
hydrophobic steroid nucleus hydrophilic lactone ring series of sugars |
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what is the hydrophobic steroid nucleus of Dig responsible for |
the rapid absorption of cardiac glycosides |
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What is the "active part" of the cardiac glycoside |
Hydrophilic lactone ring |
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what part of cardiac glycosideshas pharmacokinetic properties |
series of sugars |
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what is different about the nodal action potential |
it has no plateau |
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what phase does dig alter |
phase 4, the pacemaker potential |
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cardiac glycosides two major effects |
reversibly inhibits NA K APTase pump. Autonomic effects |
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what is responsible for the positive inotropic effect of dig |
Calcium dig does this by binding to alpha subunit of the atpase enzyme causing a conformational change, interfering with outward transport of Na. THe Na calcium antiporter system exchanges na for ca. Intracellular ca is sequestered in the SR |
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the positive inotropic effect of dig causes |
increased contractility increased SV decreased end systolic volume decreased LVEDP decreased hear size d/t less o2 consumption shift of the starling curve to the left increasesd systemic circualtion improved CO, increased renal perfusion adn exretion of fluid reduces sympathetic flow |
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a shift to the left on the frank starling curve indicates |
positive inotropic effect |
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what are the autonomic effects of dig |
-increased PSNS activity through sensitization of central arterial baroreceptors (carotid sinus) -Activation of the vagal nuclei in CNS (cardioinhibitory) |
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activation of the vagal nuclei in CNS leads to |
-decreased activity of SA node (decreasing phase 4 =slower HR) -Delayed conduction through the AV node -prolonged refractory period -slowed HR |
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EKG effects of cardiac glycosides |
prolonged PR interal (slowing through AV) shortened QT st seg depression decreased amplitude or inversion of T waves changes on ekg disappear within 20 days d/c |
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oral absorption of dig takes |
1 hour 75% is absorbed. |
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time for peak plasma concentration of dig |
1-2 hours |
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when will the effect of IV dig be seen |
5-30 minutes after IV dose, very rapid |
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Clearance of dig |
primarily kidneys, 35% excreted daily |
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elimination 1/2 time |
31-33 hours |
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how does renal dysfunction effect clearance |
delayed or slow it |
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What do you do to the dig dose if patients creat is 3-5mg/dl |
50% |
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Where is dig stored in active form and how would this effect the elderly dosage |
in the muscle tissue. so elderly with decreased muscle mass will ahve elevated plasma and cardiac levels, so decrease the dose |
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How protein bound is dig |
25%% |
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what could prevent dig from having therapeutic effects |
antibodies also, 10% of people harbor enteric bacteria that inactivate dig in gut and will therefore require a higher dose |
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how is DigiTOXIN metabolized |
by the liver, DIgoxin is one of the metabolites! |
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elimination of DigiTOXIN |
1/2 life is 5-7 days |
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does liver disease prolong elim half life? |
nope |
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OUABAIN MOA |
activates Na K ATP ase from the extracellular side, which triggers release of Ca from intracellular stores. |
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how is Ouaboin exreted |
urine |
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long or short duration of action |
short |
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is Ouabain effective orally |
no due to destruction of the glycoside portion in GI tract. |
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Digitalis therapeutic range |
NARROW 1:2.1 |
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waht is the most frequent cause of dig tox |
the presence of hypokalemia. |
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why does hypokalemia cause dig tox |
it increases cardiac glycoside binding to myocardial cells |
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if your patient takes dig in combo with what drug, you may have to watch for digitalis tox due to hypokalemia |
diuretics that cause k depletion *also watch for hyperventilating your patients on dig |
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other causes of digitalis tox |
hypercalcemia hypomag decreased muscle mass (increased plasma level) poor renal fcn (decreased clearance) |
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therapeutic digitalis range |
0.5-2.5ng/ml |
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toxic digitalis range |
3ng/ml |
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Early signs of Digitalis toicity |
****n/v and anorexia (stim of CTZ) fatigue, malaise ha trigeminal neuralgia (pain) amblyopia (blurred vision) scotomata (loss of vision Xanthopsia (disturbance of color vision) |
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with xanthopsia what happens |
patient sees yellow green color or halos pain in extremities |
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As digitalis tox prgresses, what happens |
there is a paradoxical increase in SNS outflow |
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what does the paradoxical increase in SNS outflow with progressive digitalis tox lead to |
atrial tachycardia |
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EKG changes with digitalix tox |
prolonged PR interval (delayed cond through AV) Incomplete heart block with progression to complete atrial ventricular tachyarrythmias |
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what is the MOST common arrhythmia due to digitalis tox |
atrial tachycardia with AV nodal block |
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treatment for digitalis tox |
-treat cause (possibly low K) phenytoin .5-1.5mg/kg IV over 5 min lidocaine 1-2mg/kg IV atropine 35-70mcg/kg IV propanolol or procainamide (not if conduction block present) -temp pacemaker (complete HB) cholestyamine digibind (binds to dig and carries it out, takes a while to work) |
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how does quinidine interact with digitalis |
increaes plasma concentraaitons |
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what can sympathomimetic effects with beta agonist in addition to digitalis cause |
increased chance of arrhythmias |
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how can calcium interact with digitalis |
dysrhythmias |
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how can non potassium sparing diuretics interact with digitalis |
hypokalemia |
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how can oral antacids interact with cardiac glycosides |
decrese the absorption of dig |
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how can succ theoretically interact with digitalis |
could have additive effect, due to increased PNS activity leading to brady or asytole |
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MOA of PDEIII inhibitors |
inhibit phosphodiesterase enzym -> accumulation of cAMP in myocardial cells leads to an intracellular influx of calcium ions in the cytosol (+ inotropic effects) |
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are PDEIII inhibitor catecholamines or glycosides |
nope |
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how do PDEII inhibitors effect catecholamines |
they enhance catecholamines (bc they also increase cAMP levels |
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What is the overall effect of PDEIII inhibitors |
inodilators positive inotropic effect vasodilation (venous and arterial) |
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when is a PDEIII useful |
catecholamine depletion bb'd or down regulated -on digoxin (no digitalis tox) bc works though different pathway -patients who woudl benefit from a positive inotropic effect with a reduction in SVR |
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what effect does milronone have |
positive inotropic (increased CO) and vasodilation min effect on HR and myocardial consumption |
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how do you give milrinone |
IV 50mcg/kg bolus over 10 min infusion .5mcg/kg/min |
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1/2 life milrinone |
2.7 hours
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how is milrinone excreted |
80% unchanged in urine |
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what do you do with milrinone dose with renal dysfunction GFR<50ml/min |
decrease dose to 0.375mcg/kg/min |
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When is milrinone frequently used? |
Acute LV dysfunction -post cardiac surgery or adjunct to weaning from CPB |
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when can the inotropic effects of milrinone be diminished |
with acidosis |
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Amrinone (inamrinone) drug class and dose |
PDEIII inhibitor 5-10mcg/kg min |
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what can amrinone produce with long term therapy
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thrombocytopenia |
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other PDE inhibitors like enoximone and piroximone are derivatives of |
imidazole |
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how do enoximone and piroximone work |
they act at specific pdeIII inhibitors to increase myocardial contractility |
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enoximone 1/2 life
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4.3 hours |
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enoximone metabolized |
in liver |
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enoximone dose |
0.5mg/kg IV followed by continous infusion of 5-20mcg/kg/min |
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how does amrinone effect the blood flow to kidney |
increases flow to the kidney |
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niseritide (natrecor) MOA |
increased cGMP leads to smooth muscle relaxation reduced PCWP and art BP in pts with CHF *no effects on cardiac contractlity or on measures of cardiac electrophysiology |
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dose of niseritide |
2mcg/kg IV bolus, followed by infusion of 0.01 mcg/kg/min |
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How do calcium sensitizers work |
they improve myofilament contractile response to calcium (prolong the interaction between actin and myosin filaments leading to a positive inotropic effect) -More of a contraction when they cross bridge |
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what don't calcium sensitizers do |
do not increase cAMP production do not effect calcium concentration |
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levosimendana (simdax) is what type of drug |
calcium sensitizer |
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how does simdax work |
binds to troponin C |
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benefits of simdax |
less arrrhythmias bc it doesnt change intracellular calcium -doesnt increase myocardial consumption -has selective PDEIII inhibition at higher doses |
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what order of kinetics does simdax follow |
1st order kinetics |
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1/2 life of simdax |
1 hour but has a metabolite which also has calcium sensitization effects lasting several days |
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calcium effects on contractility |
produces intense positive inotropic effect lasting 10-20 min |
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uses for calcium |
improved contractility after CPB -treat hypocalcemia d/t citrate binding after blood transfusion -treat acidosis and negative inotropic effects of acidosis |
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how much more ionized calcium per cc does a 10% solution of CaCl contain than calcium gluconate |
3x more ionized calcium per cc |
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how many mg/cc of calcium does cacl have |
27mg/cc |
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how many mg/cc of ca does calcium gluconate have |
8mg/cc |
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how long should calcium be administered over |
5-15 min |
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What is glucagon |
polypeptide hormone produced by alpha cells of pancreas |
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what does glucagon enhance the formation of |
cAMP |
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what are some uses for glucagon |
treat insulin induced hypoglycemia beta blocker reversal or overdose relaxation of sphincter of oddi HF refractory to beta 1 agonist |
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how is glucagon administered |
IV/IM only NOT PO |
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how is it infused |
1-5mg IV or infusion of 20mg/hour |
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what are the CV effects of glucagon |
increased HR increased myocardial contractility mild increase in MAP little effect of SVR |
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side effects of glucagon |
n/v hyperglycemia paradoxical hypoglycemia hypokalemia (from increased insulin) stimulation of catacholamine release (used in diagnostics of pheochromocytoma ) will cause tachy and HTN |
