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143 Cards in this Set
- Front
- Back
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Class IA antiarrhythmic & MOA |
Procainamide Quinidine (antimalarial/antiprotozoal) Dysopyramide -Blocks FAST Na channels -opens activated state -dec. APD and ERP |
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S.E. of Quinidine |
tachycardia, cinchonism (tinnitus, GI, CNS excitation, ocular dysfunction), prolonged QRS and increase QT interval -> Torsades |
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other MOA of Quinidine |
causes Muscarinic receptor blockade (inc. HR & AV conduction) vasodilate (alpha black w/ reflex tac.) |
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how is Procainamide metabolized |
via N-acetyltransferase to N-acetylprocainamide (active metabolite) |
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SE of Procainamide
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-Hypersensibility (hapten) -SLE like synd (+ ANA, + Anti-histone) -Hematotoxicity (thrombocytopenia, agranulocytosis; regular CBC) |
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Class IB & MOA |
Lidocaine Phenytoin Mexiletine Tocainide -Blocks FAST Na channels -blocks inactivated ch. |
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what antiarrhythmic will you give a patient with a recent MI or ischemic tissue? |
class Ib - lidocaine |
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how is lidocaine given and why? |
IV, bc of first-pass metabolism |
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Class IC & MOA |
Flecainide Propafenone -Blocks FAST Na ch. |
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What classes give you rhythm control? |
Class I & III |
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what classes give you rate control? |
Class II, IV & digoxin |
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what effect does beta blockers have on the heart? |
- inotropy effect decreasing oxygen demand, decreasing SA and AV nodal activity |
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What are beta blockers used for? |
prophylaxis post MI SVT |
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what class do propranolol, acebutolol and esmolol pertain to? |
Class II antiarrhythmic Beta blockers |
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what drugs pertain to class III antiarrhythmic? |
K ch. blockers (AIDS) -Amiodarone -Ibutelide -Dofetilide -Sotalol |
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What phase do Class II affect? |
decrease slope of phase 4 (diastolic current) |
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MOA of class III? |
K ch. blockers, decreaing IC K increase APD and ERP, in Purkinje and Ventricular dz |
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what phase does K ch. blockers affect? |
slows phase 3, prolonged repo |
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what are class III used for |
any arrhythmias |
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what tests do you run on patients you put on K channel blockers? |
TFT PFT |
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SE of class III |
pulmonary fibrosis thyroid dysfunction **Blue pigment on skin "smurf skin" corneal deposits hepatic necrosis |
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MOA of class IV |
Ca++ channel blocker (blocks slow cardiac Ca L-type decreasing TPR) |
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what phase do Ca ch. affect |
phase 0 phase 4 (decreasing SA & AV nodal activity) |
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name drugs in class IV |
verapamil diltiazem |
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uses of class IV |
SVT* |
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SE of verapamil and why |
constipation, bc of the blockage in the GI of calcium |
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SE of class IV |
dizziness, flushing, hypotension, AV block |
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name 3 drugs that aren't part of V. Williams classifying system |
-adenosine -magnesium -digoxin |
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DOC for Paroxysmal SVT and AV nodal arrhythmias |
adenosine |
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SE of adenosine |
flushing, sedation, dyspnea |
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what antagonizes adenosine |
methylxanthines (theophyline used in COPD also Caffeine) |
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what is magnesium used for |
torsades |
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drug preference for HTN |
alfa 1 blockers |
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alfa 1 blocker drugs |
prazosin, doxasin, terazosin |
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MOA alfa 2 agonist |
decrease sympathetic outflow ( decrease release and NE synthesis), decreasing TPR and HR |
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use of alfa 2 agonist |
mild to moderate HTN, opiate withdrawal (clonidine), *** HTN in pregnancy (methyldopa) |
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alfa 2 agonist drugs |
Methyldopa, clonidine |
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SE of alfa 2 agonist |
Positive Coombs test (methyldopa) CNS depression Edema |
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drug interaction of alfa 2 agonist |
TCA - blocks NE reuptake and 5HT |
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what drug destroys synaptic vesicle |
reserpine |
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what is the MOA of reserpine |
decrease CO and TPR decrease NE, DA, 5HT (depression) |
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SE of reserpine |
Depression (suicide) Edema increase GI secretions |
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MOA Guanethidine |
binds vesicles inhibits NE release |
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what vascular problem is associated with HTN? |
Hyaline Art. Artherosclerosis |
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SE of Guanethidine |
Diarrhea Edema |
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MOA of alfa 1 blockers |
decrease arteriolar and venous resistance, causes reflex tachicardia |
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DOC for BPH |
tamsulosin (alfa 1 blocker) |
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uses of alfa1 blockers |
HTN, BPH |
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SE of alfa1 blockers |
first dose syncope -> orthostatic hypotension, urinary incontinence |
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vasospastic disorders |
Raynaud, Prinzmetal |
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who shouldnt take Beta blockers |
asthmatics, vasospatic disorders, Diabetics |
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what drugs act through NO |
hydralazine, nitroprusside |
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MOA hydralazine |
decrease TPR via arteriolar dilation (selective) |
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SE hydralazine |
SLE like syndrome, slow acetylators, edema, reflex tachicardia (+beta blocker) |
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MOA nitroprusside |
decrease TPR via dilation of both arterioles and venules |
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Use of hydralazine |
moderate to severe HTN |
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use of nitroprusside |
ER HTN (via IV) |
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SE nitroprusside |
cyanide toxicity (do not use more than 24-36 hrs causes cyanide poisoning) |
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drugs acting to open ATP dependent K channels |
Minoxidil, diazoxide |
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MOA mof minoxidil |
open K channel, causing hyperpolarization of smooth muscle results in arteriolar vasodilation (selective) |
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uses of minoxidil & diazoxide |
ER HTN (diazoxide) severe hypertension & baldness (minoxidil) |
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SE of minoxidil & diazoxide |
hypertrichosis-excess hair growth (minoxidil) hyperglycemia (dec. insulin release - diazoxide) edema reflex tac |
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what do CCBs block |
L type Calcium channels in heart and blood vessels |
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CCB drugs |
Verapamil, diltiazem, dihydropyridine (-dipines; nifedipine) |
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uses CCB |
HTN, Angina, Antiarrhythmia (verapamil, dialtiazem) |
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SE of CCB -dipines |
reflex tac., gingival hiperplasia |
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suitable drug: Angina |
Beta blockers, CCBs |
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suitable drug: Diabetes |
ACEIs, ARBs |
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suitable drug:HF |
ACEI, ARBs, Beta blockers |
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suitable drug: post MI |
Beta blockers |
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suitable drug: BPH |
alfa blockers |
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suitable drug: Dyslipidemias |
alfa blockers, CCBs, ACEis/ARBS |
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MOA of ACEIs |
block formation of AT II by preventing of AT1 receptor stimulation dec. aldosterone and vasodilates |
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what does ACEI do to bradykinin |
prevents bradykinin degradation |
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MOA of ARBs |
block AT1 receptors |
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direct inhibitor of renin |
Aliskiren |
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MOA of aliskiren |
blocks formation of angiotensin I |
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use of ACEI and ARB |
mild to moderate HTN protective in Diabetic nephropathy CHF |
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SE of ACEI and ARB |
dry cough (ACEI) hyperkalemia (dec. aldosterone) ARF in renal artery stenosis ANgioedema ( contraindicated in C1 esterase inh def.) |
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what do you switch a patient with a dry cough under an ACEI |
ARB |
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Tx for pulmonary HTN |
bosentan sildelnafil |
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MOA of Bosentan |
Endothelin (ET) A receptor antagonist ET-1 powerful vasoconstrictor |
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SE bosentan |
headache, flushing, hypotension |
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contraindication of bosentan |
pregnancy |
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PGI2 administered via infusion pumps used for pulmonary HTN |
epoprostenol |
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decrease preload |
diuretics, ACEIs, ARBs, venodilators |
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decrease afterload |
ACEIs, ARBs, arteriodilators (hydralazine) |
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increase contractility |
digoxin, beta agonist, phosphodiesterase inhibitors (amrinone and milrinone) |
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decrease remodeling of cardic muscle |
ACEIs, ARBs, sprinolactone |
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chronic management of CHF |
ARBs, ACEIs |
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primary treatment in CHF |
~ACEI (ARB as an alternative) ~Beta blocker (metoprolol, bisoprolol, cervedilol) provide antiarrhythmic effect and decrease remodeling ~Diuretics (loop or thiazide to dec preload) (spirinolactone to block aldosterone receptor and dec remodeling) ~hydralazine + isosorbide dinitrate (preferred in pt that cant tolerate ACEI or ARBs) |
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how does dobutamine work in CHF |
beta adrenergic agonist (sympathomimetic that binds to B1 adrenoreceptors) that increases force of contraction and vasodilation via increased cAMP |
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MOA of digoxin |
direct: inh. cardiac Na/K ATPase inc. IC Ca++, inc. contractile force by inc. actin- myosin interaction indirect: inh neuronal Na/K ATPase inc vagal stimulation ( dec. HR more time for filling, Inc CO) |
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how is digoxin cleared |
renal |
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use of digoxin |
CHF, SVT |
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SE digoxin |
van gogh vision, nauseas, vomiting, diarrhea, AV block, arrhythmia <-hyperkalemia |
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antidote for digoxin toxicity |
anti-digoxin Fab antibody (Digibind), electrolytes and antiarrhythmics class IB lidocaine,phenytoin |
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drug interactions with digoxin |
verapamil, quinidine |
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phosphodiesterase inh |
Inamrinone, Milrinone |
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what NOT to give a pt with Wolff- Parkinson White syndrome |
avoid: A - adenosine B - beta blocker C- CCB D - digoxin |
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use of Nesiritide |
acutely decompensated CHF |
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MOA Nesiritide |
-binds to Natriuretic peptide receptors, -increasing ↑ cGMP -resulting in Vasodilation |
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tx for Wolff Parkinson white synd
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(A13) class Ia -Quinidine, Procainnamide, Disopyramide class III - Amiodarone, Sotalol |
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what type of angina is cause by spontaneous coronary vasospasm |
Prinzmetal |
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type of angina caused by atherosclerosis of coronary vessels and precipitated by exertion |
Classic angina |
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type of angina can be acute in onset and is caused by platelet aggregation |
Unstable angina |
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drugs that decrease oxygen demand |
↓ O2: (NBC) Nitrates, beta blockers, CCBs |
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drugs that increase oxygen demand |
↑ O2: Nitrates, CCBs |
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DOC for immediate relief of anginal symptoms |
sublingual nitroglycerin (NTG) |
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2 mechanism to treat angina |
1. inc. oxygen supply to the myocardium 2. dec. myocardial oxygen demand |
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MOA of nitrates |
Nitrates form nitrites - form NO - NO activates guanylyl cyclase to inc. cGMP- this leads to ↑ relaxation of vascular smooth muscle |
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how does cGMP relax vasc. smooth muscle |
dephosphorylation of myosin light chains |
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how do Nitrates increase oxygen demand |
dilation of coronary vessels which leads to increased blood supply |
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how do nitrates decrease oxygen demand |
dilation of large veins leads to ↓ preload - dec. preload reduce the amount of work done by the heart, dec. work of the heart results in dec. myocardial oxygen req. |
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SE of nitrates |
flushing headache orthostatic hypotension reflex tac. methemoglobinemia |
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why must pt have at least "10-12" nitrate free interval every day |
tolerance (tachyphylaxis) if given on a continuous basis |
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contraindications of nitrates pt taking what other drug |
~sildenafil ~vardenafil ~tadalafil |
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methemoglobin by amyl nitrite can be used to treat what poisoning |
cyanide |
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how do beta blockers work in treating angina |
inhibition of Beta1 adrenoreceptors leads to dec. CO, HR and force contraction, reducing the workload of the heart and oxygen demand |
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do beta blockers increase oxygen supply |
no |
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primary effects on myocardium |
verapamil, diltiazem |
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primary effects on peripheral vasculature |
-dipines (dihydropyridines) |
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how do CCBs work in treating angina |
block vasculature L type Ca++ ch. which leads to ↓ heart contractility and increase vasodilation |
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name of MC thiazide diuretic used in tx HTN |
Hydrochlorothiazide |
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what transporter is inhibited in the DCT by thiazides |
Na/ Cl transporter |
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site of action of thiazide |
DCT of nephron |
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SE of thiazides |
hyper GLUC Glycemia Lipidemia Uricemia Calcemia |
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what two types of gates does the voltage gated Na ch. have |
M (activating) H (inactivating) |
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MOA of adenosine |
stimulates Alfa1 receptors which causes decreased in cAMP (via Gi coupled) ↑ K efflux leading to increased hyperpolarization. |
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most deadly ion that can be administered |
Potassium ion |
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ECG changes in hyperkalemia |
flattened P waves; widened QRS complex; peaked T waves; sine waves; V.Fib` |
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what class Ib antiarrhythmic can cause pulmonary fibrosis |
Tocainide |
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half life of amiodarone |
40-60 days |
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T/F? lidocaine is useful in treating Atrial Arrhythmias? |
false |
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SE of Disopyramide |
anticholinergic: urinary retention; dry mouth; blurred vision; constipation; sedation |
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how should pt on amiodarone be monitored |
ECG TFT PFT LFT electrolytes ophthalmology exams |
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digoxin induced arrhythmias are treated by what drugs |
Ib: lidocaine, phenytoin |
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long QT interval puts a pt at risk for what |
Torsade de pointe, ventricular arrhythmia that can degenerate into v. fib |
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what electrolyte disturbances predispose to digoxin toxicity |
hypokalemia hypomagnesemia hypercalcemia |
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what drugs increase digoxin concentrations |
↑ : quinidine amiodarone verapamil erythromycin |
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what drugs decrease digoxin concentrations |
loop diuretics; thiazide; corticosteroids |
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how do diuretics work in CHF |
decrease intravascular vol thereby decrease in preload; reduce pulmonary and peripheral edema often seen in CHF pt. |
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which anti-arrhythmic decreases cAMP |
beta blockers |
