heart failure (sketchy)

Digoxin is a cardiac ________ used to reduce symptoms of _____________.
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Digoxin is a cardiac ________ used to reduce symptoms of _____________.
glycoside
chronic HF
_______ is the genus of plants from which cardiac glycosides are derived.
digitalis
Digitalis are natural ______ agents.
inotropic
(affecting the contraction of cardiac muscles)
Foxglove plan is a digitalis that ____ & _____ the heart
slows and strengthens
"DJ foxglove"
digoxin
digoxin aka (3)
Digitek, Digox, Lanoxin
at the molecular level, all cardiac glycosides such as _________, inhibit ______________ at the cell membrane.
digoxin
Na+-K+ ATPase
Digoxins inhibitory action of
Na+-K+ ATPase is largely responsible for the _________ effect
therapeutic effect
Digoxin increases _________ by not allowing _____ into the cell, meaning ____ can't get out.

= _________
contractility
K+
Na+

increased intracellular sodium concentration
The increased intracellular sodium concentration activates the __________, now sodium is pumped out while ________ is pumped in.

= _________
sodium-calcium exchanger
calcium

increased cytoplasmic calcium
All this increased cytoplasmic calcium leads to a rise in ________ calcium stores, resulting in ***improved _________ _________ & _______ _______ ________ function.SR *myocyte contractility *left ventricular systolicdue to digoxins ______ ______ effects, it can be used for _________ treatment of _________ _______ ________positive inotropic symptomatic chronic systolic HFdigoxin does NOT ________ ________ in patients with chronic HF, it is only used for ______ _______.reduce mortality symptomatic reliefBecause digoxin has a ________ therapeutic index, it is usually only given when _______ & ________ have failed to control symptoms.narrow diuretics & ACE inhibitorsDigoxin's NARROW therapeutic index means we also need to ?measure digoxin levelsbesides HF, Digoxn can also be used to treat certain ________.arrhythmiaDigoxn can also be used to treat certain ARRHYTHMIAS because it 1) exerts ___________ effects via ___________ _________ ________ as well as 2)facilitation of ________ transmission at the ______ ______.parasympathomimetic central vagal stimulation muscarinic cardiac myocyteDigoxin ______ stimulates the _______ , allowing treatment of certain ________ = ___________ innervationdirectly *vagus nerve arrhythmias CHOLINERGICCholinergic innervation is much richer in the _______, digoxins actions affect the ______ &_____ conduction most. this makes digoxin useful for treating ** _________ ________.atria *atria & av node ATRIAL ARRHYTHMIASFor some patients, digoxin is used to treat CHF due to _______ _______ & _______ requiring _____ _____.systolic disfunction AFIB rate controlBecause of digoxin's narrow. therapeutic index, _______ is common.toxicityAdverse effects of digoxin are related to its ______ ______, though very few occur below ______.plasmic concentration 0.8 mcg/LDigoxin toxicity =above 2 mcg/Lclassic exam scenario: A patient comes into your office on multiple medications and pmhx of HF & AFIB. One of the meds is Digoxin. What would the lab values & EKG show in Digitalis toxicity?*Elevated serum K+ levels *- premature ventricular contractions - scooped concave ST segments_________ is an important marker of digitalis (digoxin) toxicity and is even a predictor of _______.HYPERKALEMIA mortalityDigoxin is a _________ and may induce various arrhythmia during toxicity. These arrhythmias are potentially _______ so continuous _______ _______ & serial __________ are needed in the setting of toxicity.proarrhythmic fatal cardiac monitoring EKGs"digitalis effect" seen with chronic digoxin use on an EKG this consists of (4)"taSTy scoop" ** scooped/concaved ST segments 1) T wave changes 2)QT interval shortening 3)ST depression 4)prolonged PR intervalthe digitalis effect does NOT indicate ______, just _____ _____ ______toxicity long term useIf a digoxin poisoned patient arrives to your office, he's probably going to be ________ due to increased ________ activation & _________ activity at the ______ & _____ .bradycardic vagus nerve parasympathetic SA node & AV nodedigoxin toxicity can cause an ______ block.AV NODALDigoxin is contraindicated in ________ WITHOUT a _______.heart block pacemakerdigoxin should be used with caution when taken in combination with other drugs that depress sinus or AV nodal function such as ________ ______beta blockersduring acute digoxin poisoning, a patient may remain ______ for several hours, before developing significant _____ symptoms.asymptomatic GIDigoxin toxicity GI side effects:nausea vomiting abd painneurologic manifestations such as (5) are also common, especially with _____ toxicity.weakness lethargy confusion delirium disorientation chronicdigitalis toxicity can also lead to all kinds of _______ changes such as ___________ (objects appear yellow)visual changes xanthopsia______ is a HALLMARK sign of digoxin poisoning.XanthopsiaPredisposing factors to digoxin toxicity:1) hypokalemia 2) renal insufficiency 3)many antiarrythmic drugs______ exacerbates digoxin toxicityhypokalemiaHypokalemia increases digoxin binding to the _________Na+-K+ ATPasehypokalemia (exacerbating digoxin toxicity) is most commonly caused by ________ in these patients.loop diureticsrenal insufficiency can also increase patient susceptibility to digoxin toxicity by increasing it's ________ _______serum half-life_____ ______ is COMMONLY encountered in the setting of _______ digoxin toxicity and is often what causes the rise in _____ ______renal dysfunction chronic digoxin concentrationWhen dosing digoxin in a patient that has renal impairment, a ______ ______ is required.low doseassessment of ______ function is essential in these patients and should include measurements of ______&_____ as well as _____ ______ to asses renal ______.renal BUN Creatinine urine output perfusionRenal clearance of Digoxin can be inhibited by other anti arrhythmic medications (4) = ______ _______ concentrationsamiodarone verapamil diltiazem quinidine INCREASED SERUM CONCENTRATIONSThe treatment for any clinically significant arrhythmia from digoxin toxicity is ______ ______ _____ aka "_______ ______ _____"digoxin-specific antibody fragments "Digoxin immune Fab"______ _____ ____ reverses digoxin toxicity caused by extra calcium and vagal stimulation.digoxine immune FabDigoxin summary :) 1). digoxin is a _____ ______ 2) used for ______ treatment of ______ 3) it works by inhibiting _______ at the ______ _______ ______ ______ 4) inhibition causes rise in _______ _______ 5) sodium leaves the cell by _______ the _________ exchanger leading to an influx of ______ 6) more calcium = more ______ -this make digoxin useful for treating ______ _______ _______. 7) besides HF, digoxin can be used as an ______ through direct stimulation of the ________ = this affects the SA & AV node _______ causing ________ & _______ 8) Side effects of digoxin overdose include (4) 9) _______ & _______ increase susceptibility to these toxic effects 10) a ___ ____ is necessary for patients with renal dysfunction 11) The first line agent for treating clinically-significant arrhythmias from digoxin toxicity is ________1) cardiac glycoside 2) symptomatic chronic heart failure 3) Na/K ATPase cardiac myocyte cell membrane 4) intracellular sodium 5) reversing sodium-calcium CALCYUM :) 6) contractility left systolic dysfunction 7) anti-arrhythmic vagus nerve conduction BRADYCARDIA AV NODAL BLOCK 8) -elevated K+ -numerous arrythmias -gi symptoms -** glaring yellow visual disturbances (XANTHOPSIA) 9) hypokalemia renal dysfunction 10) low dose 11) Digoxin Immune-FabMagician holding a: VElvet SACk = ? floppy heart balloon=?Sacubitril/valsartan used for systolic HF_________ & _______ reduce the risk of CV death in systolic HF unlike ______.sacubitril & valsartan digoxin!ANP and BNP are _________ ________natriuretic peptidesnatruretic peptides are peptide hormones that are synthesized by the ______, _______, and other organs.heart brainANP=atrial natriuretic peptideBNP=brain natriuretic peptideThe release of ANP from the heart is stimulated by ________ _________ ________atrial ventricular distensionThe release of BNP from the brain is stimulated by ______ ______neurohumoral stimuliBoth ANP and BNP are secreted in response to _____ _____heart failureThe natriuretic peptide system counter regulates the detrimental effects of the _______ of _______ that occurs in systolic HF by producing ________ & ________up-regulation of RAAS vasodilation natriuresisexcretion of sodium in the urinenatriuresis_______ & _______ retention along with _________ is caused by 1) the activation of _______ and the _______. 2) action of _______ = ? & ?sodium & fluid vasoconstriction 1)RAAS sympathetic nervous system 2) vasopressin = INCREASED VENTRICULAR PRELOAD + AFTERLOAD & ELEVATED WALL STRESSThe increased ventricular preload & afterload stimulates _____ _____ & ________active BNP NT-pro BNPActive BNP promotes ______ & _______ wich is ______ in systemic HFnatriuresis vasodilation beneficial :)_______ _______ leads to the production of ANPatrial stretchnepalese lynx cat representsneprilysinNeprilysin is a ______ ______ that is involved in the. ________ of these vasoactive natriuretic peptides.neutral endopeptidase (NEP) degradationbradykinin has ______ properties, but _____ also metabolizes bradykinin :(vasodilator neprilysinThe magician controlling the lynx with a leash represents:Sacubitril inhibiting neprilysininhibits neprilysinsacubitrilSacubotril inhibits neprilysin, therefore the metabolism of the _______ _____ is hindered and their concentrations ________. :) = (3)vasoactive peptides increase :) 1)VASODILATION 2) reduced pre/after load 3) increased natriuresisValsartan is anARBAngiotensin 2 receptor blockervalsartansacubitril is aprodrugSacubitril is _______ but when _________ by esterases, it's converted to it's active form = ________inactive de-ethylated saculbitrilatactive form of sacubitrilsacubitrilatside affect of sacubiitril/valsartan is _______, so ______ supplements should be AVOIDEDhyperkalemia potassiumSacubitril/Valsartan can lead to (3)hypotension dizziness faintingThere is a risk of ________ & _______ with sacubitril/valsartanrenal impairment renal failurewhen giving a patient sacubitril/valsartan you should check renal function at ________ of treatment and monitor ______ ______ regularly.initiation serum creatinineanother risk of sacubitril/valsartan is ________angioedemaSacubitril/Valsartan is contraindicated with ________ due to _______ risk.ACE inhibitors angioedemacan you combine Sacubitril/Valsartan with ACE inhibitors?HELL NO!!!A ______ washout period is necessary if switching from or to an ace inhibitor to reduce the risk of angioedema.36 hour_______ is indicated for acute heart failure.MILRINONEcAMPaign sign says: "Don't Phoster Disinterest" "Mildreds the ONE" Milrinone is a ___________ inhibitor leading to decreased breakdown of _____. Mildred flexing is on the poster represents ?phosphodiesterase cAMP positive inotropic effectMilrinones increase of cAMP leads to _______ _______ which helps reduce ________ in acute HFarteriolar dilation afterloadMildreds rival campaign poster says: "NECESSARY to turn the TIDE" "BumP the GruMP" ______ is also used in acute HF. -it is a synthetic form of _______ - increases _______ in _______ muscle.Nesiritide BNP cGMP in smooth muscleNesiritide increasing cGMP leads to _____ &_____ _____ , and also causes _____ loss through diuresis.VENOUS & ARTERIAL DILATION sodium loss"Ivan the Funny's new show called DISRUPT" _______ is indicated for CHRONIC systolic HF with reduced ______ - it DISRUPTS the _____ ______ in the ____ node which reduces HR.IVABRADINE ejection fraction -funny current SAwith ivaBRADINE you should watch out for ______bradycardia