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152 Cards in this Set
- Front
- Back
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sympathetic vs parasympathetic: spinal cord segments, pregang fiber length, post gangfiber length, pregang NT, postgang NT
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sym: T1-L2, short pregang (to sym trunk), long postgang, pregang nAChR, postgang adrenergic (sweat glands are ACh); parasym: CNs III, VII, IX, X, S2-4, long pregang, short postgang, nAChR pretgang, mAChR postgang
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mAChR effects on CV: SA node, atrial myocardium, AV node, His, ventricular myocardium, systemic arterioles, systemic veins, net effects on heart, net effects on vessels
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SA node decr automaticity, atrial myocardium decr ionotropy, AV node incr refractoriness, His and ventricular myocardium have minimal effects, systemic arterioles vasodilate, systemic veins minimal effects; net heart effect causes bradycardia; net systemic effect causes decr MAP
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vagal reaction
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provoked by fear, pain, inappropriate sensitivity of carotid sinus; causes bradycardia and decr MAP (decr blood loss in emergency)
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parasympathetic agonists
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ACh (degraded rapidly); anti-AChE: edrophonium (30 sec DOA, causes GI spasms), adenosine (quick), sarin (permanant)
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edrophonium: what is it (2), used for (2), side effects
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AChE inhibitor; DOA 30 sec; side effect of abd cramping; use to incr AV nodal refractoriness for brief period (dx SVT, break certain SVT); superseded by adenosine (no GI effects)
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adenosine: what is it (2), used for (2), side effects
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AChE inhibitor; DOA 30 sec; use to incr AV nodal refractoriness for brief period (dx SVT, break certain SVT); better than edrophonium b/c no GI effects
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parasympathetic antagonists: what are they, eg. (2)
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anti mAChR: atropine (no CNS effects), scopolamine (tx motion sickness)
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atropine: what is it, used for (3), side effects
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anti mAChR; used to interrupt vagal reaction, restore AV conduction in disorders w/ AV block (inferior MI, digital intox); no CNS effects (scopalamine can tx motion sickness)
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alpha 1 receptors (3)
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constrict arterioles in kidneys, skin, GI, GU; constrict large veins; constrict GU smooth muscle
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alpha 2 receptors (2)
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constrict arterioles; platelet aggregation
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beta 1 receptors (2)
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heart: ionotropy and chronotropy (incr HR, decr refractoriness, incr velocity, incr contractility); kidney: secrete renin
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beta 2 receptors (2)
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dilate vessels in heart, skeletal muscle; dilate bronchioles
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epinephrine: receptors: effects on SVR, HR, CO, MAP
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alpha, beta1, beta2 (minor) agonist; little change in SVR b/c alpha vasoconstriction and beta2 vasodilation offset each other; incr HR b/c B1 activity overwhelms baroreceptor mediated vagal response (SVR not elevated enough to produce big vagal response); incr CO due to B1 activity (incr CO redistributed away from skin/kidney/GI towards heart/muscle); incr MAP b/c CO incr w/o SVR change
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norepinephrine: receptors: effects on SVR, HR, CO, MAP
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alpha, beta1 agonist (no beta 2); incr SVR b/c alpha constricts w/o B2 dilation; HR decr b/c B1 activation not strong enough to overcome baroreceptor mediated vagal response in response to elev SVR from alpha; CO unchanged b/c B1 opposed by vagal response due to incr SVR; MAP incr due to incr SVR w/o CO change --- powerful vasoconstrictor, minor inotrope
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dopamine: receptors: effects on SVR, HR, CO, MAP
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delta1 (low dose <2), beta1/2 (intermediate dose 2-5), alpha (high dose >5) agonist; "renal" low dose causes renal vasodilation (diuretic); "inotrope" medium dose causes incr CO (B1) w/o SVR effects (decr due to delta1 and beta2); "pressor" high dose causes NE-like effects due to alpha response swamping delta response: incr SVR, decr HR, unchanged CO, incr MAP
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phenylephrine: receptors: effects on SVR, HR, CO, MAP
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alpha agonist; incr SVR (vasoconstriction), decr HR (vagal response to incr SVR), decr CO (incr afterload), incr MAP (incr SVR)
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isoproterenol: receptors: effects on SVR, HR, CO, MAP
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beta1 and beta 2 (no alpha) agonist; decr SVR (beta-2), incr HR (beta-1, decr of vagal response b/c SVR decr), incr CO (beta-1, decr after;pad die tp decr SVR), +/- MAP -> powerful chronotrope
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dobutamine: receptors, effects on SVR, HR, CO, MAP
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selective beta1 agonist; minor decr SVR (minor beta-2 activity), minor incr HR at higher doses, large incr CO (minor decr afterload while incr inotropy), +/- MAP (poss minor incr)
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septic shock tx
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septic shock means low SVR; tx w/ phenylephrine (alpha agonist), NE (alpha agonist), high dose DA (alpha)
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cardiogenic shock tx
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cardiogenic shock means low CO; tx w/ dobutamine (beta1 only), poss high dose dopamine
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how do inotropes work?
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increase intracellular calcium -> through AC/cAMP (sympathetic agonists), through inhibition of PDE-3 (milrinone), or through inhibition of Na/K pump (digoxin); also works to incr NE (stimulate release, block reuptake)
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primary MOA of digoxin
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inhibits Na/K pump -> [Na]i rises -> Na/Ca pump shuttles more Na out and Ca in -> [Ca]i rises
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how does digoxin shift Starling curve?
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upward and leftward (more SV, less LV filling P)
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therapeutic dose of digoxin - effects (2)
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increased inotropy w/o incr HR; no desensitization
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what inotropes don't desensitize?
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digoxin, PDE-3 inhibitors (milrinone)
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digoxin: half-life, elimination, ther. level
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half life 36 hrs; renal (80%) excretion, .5-1 therapeutic level (above = arrhythmias)
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digoxin effects on: CO, LVEF, LVEDP, exercise tolerance, natriuresis
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incr CO, incr LVEF, decr LVEDP, incr exercise tolerance, incr natriuresis
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digoxin effects on: plasma NE, PNS activity, RAAS activity, vagal tone, arterial baroreceptors
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decr NE, decr PNS activity, decr RAAS (CO incr therefore kidneys decr RAAS), incr vagal tone (-> decr HR), normalized arterial baroreceptors
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SA node: digoxin ther, toxic effects
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ther: slowing sinus rate (vagotonic); toxic: sinus arrest or SA exit block
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atrial myocardium: digoxin ther, toxic effects
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ther: not much; toxic: conduction slowing (vagal), predisposition to automatic impulse initiation (delayed after depolarization-> ATs)
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AV node: digoxin ther, toxic effects
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ther: prolongation of AV conduction (vagal and direct -> cause incr refractory period); toxic: AV block (can counteract w/ atropine -> anti-mAChR)
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Purkinje and ventricular myocardium: digoxin ther, toxic effects
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ther: prolong AP -> inotropy (more Ca); toxic: delayed after depolarization -> VTs
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long term effects of digoxin
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survival similar to placebo, but fewer hospital admissions for HF (better QOL) - instead, pts died of arrhythmias and MIs
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clinical uses of digoxin
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atrial fibrillation w/ rapid ventricular response (block AV node transmission of fibrillation - must avoid in WPW pts); CHF sx despite medical therapy (not first line therapy for CHF anymore)
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contraindications of digoxin (5)
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advanced AV block w/o pacemaker (can worsen); bradycardia w/o pacemaker (can worsen); PVCs or VT (can worsen); hypokalemia (incr digoxin effects); WPW w/ AF (will cause VF since AV node will be delayed)
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digoxin toxicity: what systems (5), what effects (3 each)
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cardiac: arrhythmias, blocks, CHF exacerbation (secondary to heart block or bradycardia); GI: nausea, vomiting, diarrhea; nervous: depression, disorientation, paresthesaias; visual: blurred vision, halos, yellow-green vision; hyperestrogenism: gynecomastia, galactorrhea
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what imbalances predispose to digoxin toxicity
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hypokalemia (potassium competes w/ digoxin for Na/K pump); hypomagnesemia; hypothyroidism; hypoxia
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tx of digoxin toxicity
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Fab antibody fragment directed against digoxin
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DA1 receptor
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vasodilation of renal, mesenteric, coronary, cerebral beds
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DA2 receptor
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inhibits reuptake of NE -> indirect beta stimulation
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dopamine indications (3)
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renal dose (<2) used for diuresis; inotrope dose (2-5) used for HF w/o hypotension; pressor dose (>5) used for HF w/ severe hypotension or cardiogenic shock
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dopamine side effects (4)
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tachycardia w/ high dose; HTN with high dose; nausea/vomiting; infiltration of IV site -> vasoconstriction -> gangrene/necrosis
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sympathetic vs parasympathetic: spinal cord segments, pregang fiber length, post gangfiber length, pregang NT, postgang NT
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sym: T1-L2, short pregang (to sym trunk), long postgang, pregang nAChR, postgang adrenergic (sweat glands are ACh); parasym: CNs III, VII, IX, X, S2-4, long pregang, short postgang, nAChR pretgang, mAChR postgang
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dobutamine side effects (6)
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arrhythmias; ischemia/angina (used for dx); hypotension (less common); tachycardia (w/ incr dose); rapid ventricular response in AF (incr AV conduction rate); nausea, headache, palpitations
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mAChR effects on CV: SA node, atrial myocardium, AV node, His, ventricular myocardium, systemic arterioles, systemic veins, net effects on heart, net effects on vessels
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SA node decr automaticity, atrial myocardium decr ionotropy, AV node incr refractoriness, His and ventricular myocardium have minimal effects, systemic arterioles vasodilate, systemic veins minimal effects; net heart effect causes bradycardia; net systemic effect causes decr MAP
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what do we use to phamacologically stimulate exercise?
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dobutamine
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vagal reaction
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provoked by fear, pain, inappropriate sensitivity of carotid sinus; causes bradycardia and decr MAP (decr blood loss in emergency)
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epinephrine side effects (4)
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tachycardia; ischemia; platelet aggregation and infarction (as a result, clinical usage declined); anxiety, fear, restlessness
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parasympathetic agonists
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ACh (degraded rapidly); anti-AChE: edrophonium (30 sec DOA, causes GI spasms), adenosine (quick), sarin (permanant)
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isoproternol indications (1)
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beta agonist (powerful chronotrope) -> used almost exclusively after heart transplant to drive HR of denervated heart and decr pulmonary vascular resistance
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edrophonium: what is it (2), used for (2), side effects
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AChE inhibitor; DOA 30 sec; side effect of abd cramping; use to incr AV nodal refractoriness for brief period (dx SVT, break certain SVT); superseded by adenosine (no GI effects)
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PDE-3 inhibitors effects (6)
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increase contractility independently of beta receptors; no increase of HR at low dose; vasodilator in both veins and pulm vessels (decr preload and afterload); improved exercise tolerance; inhibits platelet aggregation; anti-inflammatory (anti-cytokines)
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adenosine: what is it (2), used for (2), side effects
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AChE inhibitor; DOA 30 sec; use to incr AV nodal refractoriness for brief period (dx SVT, break certain SVT); better than edrophonium b/c no GI effects
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PDE-3 inhibitors cautions (1)
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severe hypotension can occur if filling pressures not elevated
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parasympathetic antagonists: what are they, eg. (2)
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anti mAChR: atropine (no CNS effects), scopolamine (tx motion sickness)
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currently available PDE-3 inhibitors
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amnirone (don't use b/c causes thrombocytopenia), milrinone; both only available IV
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atropine: what is it, used for (3), side effects
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anti mAChR; used to interrupt vagal reaction, restore AV conduction in disorders w/ AV block (inferior MI, digital intox); no CNS effects (scopalamine can tx motion sickness)
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amnirone
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IV-only PDE-3 inhibitor (milrinone preferred b/c amnirone causes thrombocytopenia)
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alpha 1 receptors (3)
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constrict arterioles in kidneys, skin, GI, GU; constrict large veins; constrict GU smooth muscle
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alpha 2 receptors (2)
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constrict arterioles; platelet aggregation
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milrinone
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IV-only PDE-3 inhibitor (preferred over amnirone, oral causes incr mortality)
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beta 1 receptors (2)
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heart: ionotropy and chronotropy (incr HR, decr refractoriness, incr velocity, incr contractility); kidney: secrete renin
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vesnarinone
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oral PDE-3 inhibitor; not approved due to incr mortality
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beta 2 receptors (2)
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dilate vessels in heart, skeletal muscle; dilate bronchioles
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enoximone
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oral PDE-3 inhibitor; not approved due to incr mortality at high doses and little effectiveness at low doses
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epinephrine: receptors: effects on SVR, HR, CO, MAP
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alpha, beta1, beta2 (minor) agonist; little change in SVR b/c alpha vasoconstriction and beta2 vasodilation offset each other; incr HR b/c B1 activity overwhelms baroreceptor mediated vagal response (SVR not elevated enough to produce big vagal response); incr CO due to B1 activity (incr CO redistributed away from skin/kidney/GI towards heart/muscle); incr MAP b/c CO incr w/o SVR change
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beta agonists vs PDE-3 inhibitors: pros (1 for beta, 5 for PDE3) and cons (5 for beta, 5 for PDE3)
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beta agonists increase contractility but are only weak vasodilators, weaken diastolic fn (?) arrhythmias, tachycardia, desensitization; PDE3 inhibitors incr contracility, improve diastolic fn (?), veno/vasodilator, no desensitization, can use w/ beta blockers, but they are also pro-arrhythmic, cause tachycardia, hypotension, thrmobocytopenia (amnirone more commonly), and have a longer half life (need bolus dose?)
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norepinephrine: receptors: effects on SVR, HR, CO, MAP
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alpha, beta1 agonist (no beta 2); incr SVR b/c alpha constricts w/o B2 dilation; HR decr b/c B1 activation not strong enough to overcome baroreceptor mediated vagal response in response to elev SVR from alpha; CO unchanged b/c B1 opposed by vagal response due to incr SVR; MAP incr due to incr SVR w/o CO change --- powerful vasoconstrictor, minor inotrope
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tachyphylaxis
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desensitization
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dopamine: receptors: effects on SVR, HR, CO, MAP
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delta1 (low dose <2), beta1/2 (intermediate dose 2-5), alpha (high dose >5) agonist; "renal" low dose causes renal vasodilation (diuretic); "inotrope" medium dose causes incr CO (B1) w/o SVR effects (decr due to delta1 and beta2); "pressor" high dose causes NE-like effects due to alpha response swamping delta response: incr SVR, decr HR, unchanged CO, incr MAP
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when to give acute and chronic inotropic IV therapy (3)
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acute: decompensated w/ V overload and impaired perfusion; chronic: bridge to transplant, or palliation (refractory HF sx after max medical therapy -> will incr mortality but also incr QOL)
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phenylephrine: receptors: effects on SVR, HR, CO, MAP
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alpha agonist; incr SVR (vasoconstriction), decr HR (vagal response to incr SVR), decr CO (incr afterload), incr MAP (incr SVR)
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alpha antagonists: used to tx (3), fn, drugs (3)
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used to tx HTN (third line), BPH, and improve voiding in pts w/ bladder outlet obstruction; cause arteriolar and venodilation -> decr SVR; Prazosin (alpha 1 > alpha 2 antagonist), Doxazosin or Terazosin (pure alpha 1 blockers, longer half lives)
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isoproterenol: receptors: effects on SVR, HR, CO, MAP
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beta1 and beta 2 (no alpha) agonist; decr SVR (beta-2), incr HR (beta-1, decr of vagal response b/c SVR decr), incr CO (beta-1, decr after;pad die tp decr SVR), +/- MAP -> powerful chronotrope
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prazosin: what is it, used to tx (3), pharmacokinetics
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alpha 1 > alpha 2 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; shorter onset and duration than doxazosin/terazosin
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dobutamine: receptors, effects on SVR, HR, CO, MAP
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selective beta1 agonist; minor decr SVR (minor beta-2 activity), minor incr HR at higher doses, large incr CO (minor decr afterload while incr inotropy), +/- MAP (poss minor incr)
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doxazosin: what is it, used to tx (2), pharmacokinetics
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alpha 1 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; longer onset and duration than prazosin
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septic shock tx
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septic shock means low SVR; tx w/ phenylephrine (alpha agonist), NE (alpha agonist), high dose DA (alpha)
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terazosin: what is it, used to tx (2), pharmacokinetics
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alpha 1 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; longer onset and duration than prazosin
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cardiogenic shock tx
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cardiogenic shock means low CO; tx w/ dobutamine (beta1 only), poss high dose dopamine
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beta blockers used to tx (4)
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CHF, MI/angina, arrhythmias, HTN
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how do inotropes work?
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increase intracellular calcium -> through AC/cAMP (sympathetic agonists), through inhibition of PDE-3 (milrinone), or through inhibition of Na/K pump (digoxin); also works to incr NE (stimulate release, block reuptake)
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propranolol: function, lipophilicity, oral or IV, DOA/formulations, price
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nonselective beta blocker (beta 1 and beta 2) - can't be used in lung dis pts; lipophilic (CNS activity -> tx migraine, causes dreams); oral and IV; short or long DOA (standard and sustained release); cheap
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primary MOA of digoxin
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inhibits Na/K pump -> [Na]i rises -> Na/Ca pump shuttles more Na out and Ca in -> [Ca]i rises
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metoprolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective beta blocker (can use in lung dis pts); moderately lipophilic (CNS activity -> tx migraines, cause dreams); oral and IV; short or long DOA (standard and sustained release); relatively cheap
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how does digoxin shift Starling curve?
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upward and leftward (more SV, less LV filling P)
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atenolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective beta blocker (can use in lung dis pts); not lipophilic (no CNS activity); oral only; intermediate DOA (6-7 hrs -> dose 2/day); standard formulation (no sustained-release); relatively cheap
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esmolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective blocker (can use in lung dis); ultra short DOA (continuous IV only); very expensive; not lipophilic (no CNS activity); use when acute reversible beta blockade needed
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therapeutic dose of digoxin - effects (2)
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increased inotropy w/o incr HR; no desensitization
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carvedilol: function, lipophilicity, oral or IV, DOA/formulations, price
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combined beta blocker (beta 1, beta 2, alpha); moderately lipophilic (some CNS activity); oral only; long DOA; standard and sustained release; expensive
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what inotropes don't desensitize?
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digoxin, PDE-3 inhibitors (milrinone)
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tx of cardiogenic shock
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inotrope -> don't use beta blockers in decompensated HF; can give beta blockers after pt is compensating again
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digoxin: half-life, elimination, ther. level
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half life 36 hrs; renal (80%) excretion, .5-1 therapeutic level (above = arrhythmias)
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why give beta blockers to CHF pt?
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beta blockers prevent RAAS activation (and therefore prevent vasoconstriction and water retention, incr afterload on heart)
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digoxin effects on: CO, LVEF, LVEDP, exercise tolerance, natriuresis
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incr CO, incr LVEF, decr LVEDP, incr exercise tolerance, incr natriuresis
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beta blockers in MI
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give pt beta blockers w/in 1 hr of MI for max effect (reduce myocardial O2 demand); however, don't give if complete heart block
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digoxin effects on: plasma NE, PNS activity, RAAS activity, vagal tone, arterial baroreceptors
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decr NE, decr PNS activity, decr RAAS (CO incr therefore kidneys decr RAAS), incr vagal tone (-> decr HR), normalized arterial baroreceptors
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why give beta blockers to angina pt?
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most endocardial perfusion occurs during diastole, and diastole is shortened and has higher diastolic BP during tachycardia and HTN; therefore, to prevent decr coronary perfusion, give beta blockers to decr HR and decr BP (and thus incr diastolic perfusion), as well as to decr myocardial O2 demand
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SA node: digoxin ther, toxic effects
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ther: slowing sinus rate (vagotonic); toxic: sinus arrest or SA exit block
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centrally acting alpha 2 agonists: drugs (2), fn, use to tx, side effects
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methyldopa, clonidine; stimulate pregang alpha2 receptors on adrenergic neurons in medulla -> reduces symp outflow, leaving unopposed vagal tone -> used to tx HTN (decr PVR, HR, CO, BP); side effects due to vagal tone (dry mouth, orthostatic hypotension, bradycardia, somnolence, etc., also causes rebound HTN w/ discontinuation)
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atrial myocardium: digoxin ther, toxic effects
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ther: not much; toxic: conduction slowing (vagal), predisposition to automatic impulse initiation (delayed after depolarization-> ATs)
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methyldopa
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centrally acting alpha 2 agonist used to tx HTN; utility limited by CNS depressant effect
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AV node: digoxin ther, toxic effects
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ther: prolongation of AV conduction (vagal and direct -> cause incr refractory period); toxic: AV block (can counteract w/ atropine -> anti-mAChR)
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clonidine
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centrally acting alpha 2 agonist used to tx HTN; given by mouth 2/day or transdermal path 1/week
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Purkinje and ventricular myocardium: digoxin ther, toxic effects
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ther: prolong AP -> inotropy (more Ca); toxic: delayed after depolarization -> VTs
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reserpine
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1st drug used to tx HTN; depletes peripheral NE from storage vesicles -> decr PVR; takes 2-3 weeks for max effects; major side effect is CNS depression and severe orthostatic hypotension (not used anymore)
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long term effects of digoxin
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survival similar to placebo, but fewer hospital admissions for HF (better QOL) - instead, pts died of arrhythmias and MIs
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adrenergic NT blockers (2)
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reserpine, guanethidine
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clinical uses of digoxin
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atrial fibrillation w/ rapid ventricular response (block AV node transmission of fibrillation - must avoid in WPW pts); CHF sx despite medical therapy (not first line therapy for CHF anymore)
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guanethidine
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decr NE release from peripheral SNS nerve endings -> tx HTN; side effect of orthostatic hypotension
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contraindications of digoxin (5)
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advanced AV block w/o pacemaker (can worsen); bradycardia w/o pacemaker (can worsen); PVCs or VT (can worsen); hypokalemia (incr digoxin effects); WPW w/ AF (will cause VF since AV node will be delayed)
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digoxin toxicity: what systems (5), what effects (3 each)
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cardiac: arrhythmias, blocks, CHF exacerbation (secondary to heart block or bradycardia); GI: nausea, vomiting, diarrhea; nervous: depression, disorientation, paresthesaias; visual: blurred vision, halos, yellow-green vision; hyperestrogenism: gynecomastia, galactorrhea
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what imbalances predispose to digoxin toxicity
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hypokalemia (potassium competes w/ digoxin for Na/K pump); hypomagnesemia; hypothyroidism; hypoxia
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tx of digoxin toxicity
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Fab antibody fragment directed against digoxin
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DA1 receptor
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vasodilation of renal, mesenteric, coronary, cerebral beds
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DA2 receptor
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inhibits reuptake of NE -> indirect beta stimulation
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dopamine indications (3)
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renal dose (<2) used for diuresis; inotrope dose (2-5) used for HF w/o hypotension; pressor dose (>5) used for HF w/ severe hypotension or cardiogenic shock
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dopamine side effects (4)
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tachycardia w/ high dose; HTN with high dose; nausea/vomiting; infiltration of IV site -> vasoconstriction -> gangrene/necrosis
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dobutamine side effects (6)
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arrhythmias; ischemia/angina (used for dx); hypotension (less common); tachycardia (w/ incr dose); rapid ventricular response in AF (incr AV conduction rate); nausea, headache, palpitations
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what do we use to phamacologically stimulate exercise?
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dobutamine
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epinephrine side effects (4)
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tachycardia; ischemia; platelet aggregation and infarction (as a result, clinical usage declined); anxiety, fear, restlessness
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isoproternol indications (1)
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beta agonist (powerful chronotrope) -> used almost exclusively after heart transplant to drive HR of denervated heart and decr pulmonary vascular resistance
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PDE-3 inhibitors effects (6)
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increase contractility independently of beta receptors; no increase of HR at low dose; vasodilator in both veins and pulm vessels (decr preload and afterload); improved exercise tolerance; inhibits platelet aggregation; anti-inflammatory (anti-cytokines)
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PDE-3 inhibitors cautions (1)
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severe hypotension can occur if filling pressures not elevated
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currently available PDE-3 inhibitors
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amnirone (don't use b/c causes thrombocytopenia), milrinone; both only available IV
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amnirone
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IV-only PDE-3 inhibitor (milrinone preferred b/c amnirone causes thrombocytopenia)
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milrinone
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IV-only PDE-3 inhibitor (preferred over amnirone, oral causes incr mortality)
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vesnarinone
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oral PDE-3 inhibitor; not approved due to incr mortality
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enoximone
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oral PDE-3 inhibitor; not approved due to incr mortality at high doses and little effectiveness at low doses
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beta agonists vs PDE-3 inhibitors: pros (1 for beta, 5 for PDE3) and cons (5 for beta, 5 for PDE3)
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beta agonists increase contractility but are only weak vasodilators, weaken diastolic fn (?) arrhythmias, tachycardia, desensitization; PDE3 inhibitors incr contracility, improve diastolic fn (?), veno/vasodilator, no desensitization, can use w/ beta blockers, but they are also pro-arrhythmic, cause tachycardia, hypotension, thrmobocytopenia (amnirone more commonly), and have a longer half life (need bolus dose?)
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tachyphylaxis
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desensitization
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when to give acute and chronic inotropic IV therapy (3)
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acute: decompensated w/ V overload and impaired perfusion; chronic: bridge to transplant, or palliation (refractory HF sx after max medical therapy -> will incr mortality but also incr QOL)
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alpha antagonists: used to tx (3), fn, drugs (3)
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used to tx HTN (third line), BPH, and improve voiding in pts w/ bladder outlet obstruction; cause arteriolar and venodilation -> decr SVR; Prazosin (alpha 1 > alpha 2 antagonist), Doxazosin or Terazosin (pure alpha 1 blockers, longer half lives)
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prazosin: what is it, used to tx (3), pharmacokinetics
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alpha 1 > alpha 2 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; shorter onset and duration than doxazosin/terazosin
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doxazosin: what is it, used to tx (2), pharmacokinetics
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alpha 1 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; longer onset and duration than prazosin
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terazosin: what is it, used to tx (2), pharmacokinetics
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alpha 1 antagonist -> used to tx HTN (third line) by causing arteriolar and venodilation, also used to improve voiding in pts w/ urinary bladder outlet obstruction (alpha receptors vasoconstrict GU sys) and to tx BPH; longer onset and duration than prazosin
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beta blockers used to tx (4)
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CHF, MI/angina, arrhythmias, HTN
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propranolol: function, lipophilicity, oral or IV, DOA/formulations, price
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nonselective beta blocker (beta 1 and beta 2) - can't be used in lung dis pts; lipophilic (CNS activity -> tx migraine, causes dreams); oral and IV; short or long DOA (standard and sustained release); cheap
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metoprolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective beta blocker (can use in lung dis pts); moderately lipophilic (CNS activity -> tx migraines, cause dreams); oral and IV; short or long DOA (standard and sustained release); relatively cheap
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atenolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective beta blocker (can use in lung dis pts); not lipophilic (no CNS activity); oral only; intermediate DOA (6-7 hrs -> dose 2/day); standard formulation (no sustained-release); relatively cheap
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esmolol: function, lipophilicity, oral or IV, DOA/formulations, price
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beta-1 selective blocker (can use in lung dis); ultra short DOA (continuous IV only); very expensive; not lipophilic (no CNS activity); use when acute reversible beta blockade needed
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carvedilol: function, lipophilicity, oral or IV, DOA/formulations, price
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combined beta blocker (beta 1, beta 2, alpha); moderately lipophilic (some CNS activity); oral only; long DOA; standard and sustained release; expensive
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tx of cardiogenic shock
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inotrope -> don't use beta blockers in decompensated HF; can give beta blockers after pt is compensating again
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why give beta blockers to CHF pt?
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beta blockers prevent RAAS activation (and therefore prevent vasoconstriction and water retention, incr afterload on heart)
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beta blockers in MI
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give pt beta blockers w/in 1 hr of MI for max effect (reduce myocardial O2 demand); however, don't give if complete heart block
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why give beta blockers to angina pt?
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most endocardial perfusion occurs during diastole, and diastole is shortened and has higher diastolic BP during tachycardia and HTN; therefore, to prevent decr coronary perfusion, give beta blockers to decr HR and decr BP (and thus incr diastolic perfusion), as well as to decr myocardial O2 demand
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centrally acting alpha 2 agonists: drugs (2), fn, use to tx, side effects
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methyldopa, clonidine; stimulate pregang alpha2 receptors on adrenergic neurons in medulla -> reduces symp outflow, leaving unopposed vagal tone -> used to tx HTN (decr PVR, HR, CO, BP); side effects due to vagal tone (dry mouth, orthostatic hypotension, bradycardia, somnolence, etc., also causes rebound HTN w/ discontinuation)
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methyldopa
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centrally acting alpha 2 agonist used to tx HTN; utility limited by CNS depressant effect
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clonidine
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centrally acting alpha 2 agonist used to tx HTN; given by mouth 2/day or transdermal path 1/week
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reserpine
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1st drug used to tx HTN; depletes peripheral NE from storage vesicles -> decr PVR; takes 2-3 weeks for max effects; major side effect is CNS depression and severe orthostatic hypotension (not used anymore)
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adrenergic NT blockers (2)
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reserpine, guanethidine
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guanethidine
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decr NE release from peripheral SNS nerve endings -> tx HTN; side effect of orthostatic hypotension
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