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DIT cardiophysquiz+
antiarrhymics too
| Question | Answer |
|---|---|
| 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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