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DIT cardiophysquiz+

antiarrhymics too

phase 0 myocardial AP rapid upstroke: sodium channels open
phase 1 myocardial AP initial repolarization: inactivation of sodium channels, K+ start to open.
phase 2 myocardial AP plateau: open K+ are balanced by Ca++ influx
phase 3 myocardial AP rapid repolarization: Ca++ closure, massive K+ efflux
phase 4 myocardial AP resting potential: High K premeability through K+ channels
MAP 1/3sys + 2/3 dia
PP sys-dia
Cardiac Output = SV x HR
Cardiac Output = rate of O2 consumption/ (arterial O2 - venous O2)
what factors affect stroke volume? contractility, afterload, preload
what heart sound is a/w dilated congestive HF? S3
what heart sound is a/w chronic HTN S4
jugular venous a wave atrial contraction
jugular venous c wave RV contraction
jugular venous x wave tricuspid closure
jugular venous v wave max. atrial filling
jugular venous y wave passive emptying of RA into RV
Ejection fraction = SV/EDV
what phys accounts for the automaticity of the AV and SA nodes phase 4 gradual sodium conduction
with what type of congenital heart defect would increasing afterload be beneficial R to Left shunts : T of F, Transposition, Truncus Arteriosus and Eisenmenger
Where does the QRS complex fall in relation to valvular dynamics? mitral valve closure
when does isovolumetric contraction take place? during QRS after MV closes before AV opens
focal myocardial inflammation with multinecleate giant cells Aschoff bodies
eosinophilic, cytoplasmic globules in liver near nucleus mallory bodies
desquamated epithelial casts in sputum curshmann's spirals (bronchial asthma)
How does HF create edema increased capillary pressure
how does liver failure create edema decreased production of proteins = decreased capillary oncotic pressure
how do infections and toxins create edema increased capillary permeability
how does lymphatic block create edema protein retention in tissue = increased interstitial oncotic pressure
Mobitz I 2nd degree AV block PR interval gets longer and longer until the beat drops
mobitz II 2nd degree AV block beat drops reandomly
Class I antiarrhytmic Na channel blockers
Class II antiarrhythmic beta blockers
Class III antiarrhythmic K+ channel blockers
Class IV antiarrhythmics Ca++ channel blockers
what stimulates myosin light-chain kinase calmodulin/ca complex
what inhibits MLCK cAMP ( via epibeta2, PGE2)
how does hypotension cause reflex tachycardia carotid sinuse sense low BP - less stim of baroreceptor - less stim of glossopharyngeal n - solitary tract of medulla - increased symp/decrease PS
Class IA Procainamide, Quinidine, Disopyrmaide
treats wolff-parkinson-white syndrome procainamide, amiodarone
phase 0 and phase 3 effects class I drugs
increases ERP out of all class I drugs class Ia
decreases ERP (class I drugs) Ib> Ic
Class IB Tocainide, Lidocaine, Mexiletine
slow HR down, used in acute ventricular tachyarrhythmias Class Ib
best post MI Class Ib
contraindicated post MI Class Ic
Class IC Flecainide, Encainide, Propafenone
affect phase 4 to suppress abnormal pacemakers Class II (beta blockers)
affect phase 3, elongates refractory period Class III (K+ blockers)
rhythm control for AFib Class III (K+ blockers)
SE: pulmonary fibrosis, heptotoxicity, hypo/hyperthyroidism, corneal deposits, gray man, photodermatitiis, neuro, constipation, CV amiodarone
check PFTs, LFTs, TFTs amiodarone
Affect phase 2, used for SVT prevention Class IV (Ca blockers)
drug of choice in diagnosing/abolishing SVT adenosine
reversed by theophylline adenosine
work at vessels, not at heart Dihydropyridine Ca channel blockers (nifedipine)
acidosis and K+ causes hyperkalemia
Created by: kayjames



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