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ECG features of PVCs   wide, bizarre QRS, don't see P wavesb bc within QRS  
tx for A fib   1) unstable: cardiovert; 2) stable: rate control w CCB, cardiovert (but if >48hrs either need to use TEE to check for clot or anticoag 3 wks, then cardiovert…continue 4 wks anticoag after  
atrial and ventricular rate for A fib   atrial ~400, ventricular 75-175  
atrial and ventricular rate for A flutter   atrial: 250-350, ventricular: 1/2 to 1/3  
name arrhythm: saw-tooth baseline w QRS every 2-3   A flutter  
MC cause A flutter   COPD  
long term tx of A fib   rate control w b-blocker or CCB, anti coag (exc if no heart dz <60)  
dzs/causes assoc w A Fib   PIRATES: Pulmon, Isch, RHD, Anemia/atrial myxoma, Thyroid, EtOH, Sepsis…also post-op stress, and pericarditis/pericardial trauma(sx)  
differentiate A fib, A flutter, and MAT based on p-waves   Afib: no distinct p waves, Aflutter: saw tooth, MAT: at least 3 difft morph of P waves  
tx MAT   if nml LV fxn: verapamil, b block; if abnml fxn digoxin, diltiazem, amiodarone  
MAT usu assoc w   severe pul dz, ie COPD  
how pathophysiol difft AVNRT and AVRT   in AVNRT the access path is within the AV node; in AVRT the path conducts retrograde  
how are pwaves difft AVNRT v AVRT   in AVNRT p wave is in QRS, so don't see it; AVRT may see p-wave after QRS  
tx of AVNRT   vagal maneuvers, IV adenosine (cardiovert if Rx doesn't work); longterm: digoxin (+/- radiofreq ablation)  
tx of AVRT   same as AVNRT  
describe ECG of WPW   narrow QRS w delta wave, short PR  
what Rx can use for WPW, can NOT use   can use procainamide or quinidine; can NOT use Rx that work on AV node (digoxin, verapamil)  
tx WPW   can use procainamide or quinidine, then radiofreq ablation  
pathophysiol of WPW   accessory path from atria to ventricle, so don't have AV node delay  
how define VT   3 or more PVC in a row  
describe ECG of VT   nml P waves dissoc from wide, bizarre QRS that can be of the same or difft morphs  
tx of nonsustained VT   if <30 sec and sympt, no tx nec; but look closely for heart dz; if heart dz do electrophysiol and if inducible, sustained VT then place ICD  
MC causes VT   CAD w prior MI, also prolonged QT  
if can't place an ICD for VT, what Rx use longterm   amiodarone  
tx sustained VT   if hemo stable, SBP>90, mild symot: IV amiodarone; if unstable: synch cardiovert then IV amiodaron  
longterm tx of sustained VT   ICD, unless nml LV fxn: amiodarone  
risk of sustained VT   can progress to Vfib  
rate of VT   100-250  
ECG of Vfib   no waves, very irreg rhythm  
acute tx Vfib   1) unsynch cardiovert, up to 3 assess rhythm after ea; 2) if persists then IV epi (1mg q3-5min); 3) if refractory then IV amiodarone followed by shock; once rhythm continue IV amiodarone or the Rx that worked  
chronic tx Vfib   if <48hrs of acute MI, no chronic tx; if not assoc MI: ICD (or amiodarone 2nd line)  
tx torsades de pointes   IV Mg++  
what is torsdes de pointes assoc w   long QT (can lead to Vfib)  
how is stable angina managed acutely   ASA, b-blocker, nitrate (+/- CCB)  
how is stable angina managed chronically   same as acutely: ASA, b-blocker, nitrate (+/- CCB)  
how is unstable angina managed acutely   IV access, O2, ASA, nitrate, morphine, b-blocker, heparin [LMWH enoxoparin is best] **so same as stable angina chronic tx + heparin  
how is acute MI tx Rx   same as unstable angina [IV access, O2, ASA, nitrate, morphine, b-blocker, heparin/LMWH + ACEI and statins  
how is MI tx after acute phase   ASA, b-block, nitrate, ACEI, statins (so same as angina but also statin and ACEI)  
how is acute CHF tx   IV access, O2, diurese, ACEI, **NOT b-blocker  
how is CHF tx based on NYHA   NYHA I, II: Na restrict, diuretic, ACEI; II-II: add b-blocker; II-IV: digoxin +/- spironolactone [if isch then also need ASA and statin +/- nitrates]  
what Rx are used for pharmacol stress test and how do they work   dobutamine (incrses HR, BP, contractility, so incrses cardiac demand), adenosine and dipyramidole (vasodilate, dz'd vessels already dilated so they get relatively less blood)  
when is CABG indicated   1) L main, 2) 3 vessel and decrsd EF, 3) 2 vessel and prox LAD  
define unstable angina   incrsd in freq, duration or intensity of angina, angina at rest  
name glycoprotein Iib/IIIa inhib   abciximab, tirofiban  
what is a tx specific to hyperhomocystenemia   folate  
should thrombolytics or CCB be used in unstable angina   haven't been shown to be beneficial, so no  
how manage dx of unstable angina   give medical tx, if respond send for stress ECG, otherwise send to cath  
how confirm Prinzmetal's angina   during cor angiography give IV ergonovine and it will cause symptoms  
how does Prinzmetal's angina present   angina at rest, ST elevation during episodes, but negative cardiac enzymes  
what defines a + stress test   ST segment depression (subendo isch), hypotension, chest pain, arrhythmias, onsert CHF  
define stable angina   pain 1-5 min (<15min), comes on w exertion or emotion, relived w NG or rest  
how differentiate unstable angina and NSTEMI   NSTEMI has positive cardiac enzymes  
what ECG changes would you see early in a MI, but not later   peaked T  
what ECG changes are seen late after MI   Q waves (specific for necrosis)  
what 4 ECG changes are seen w MI   peaked T, ST elevation, T wave inversion, Q waves  
describe timing for cardiac enzyme elev   CK-MB: rises 4-8h, peak 24h, nml 48-72h; TnI, T: rises 3-5h, peak 24-48h, nml 5-14d  
when test cardiac enzymes (how often)   on admission and q8h for 24h  
what condition can incrs Tn I   renal failure  
what are indications for thrombolysis in MI   ST elev in 2 contiguous ECG leads w pain onset <6 h that doesn't respond to NG  
what are contraindications for thrombolysis in MI   HTN >180/110, recent head trauma or traumatic CPR, active PUD, h/o stroke, recent surgery or invasive procedure, dissection Ao aneurysm  
what ECG changes seen in anterior infarct   ST elev in V1-4 (Acute) that become Q late  
what ECG changes seen in posterior infarct   large R, ST depress, and upright and prominent T in V1,2  
what ECG changes seen in lateral infarct   Q in I and aVL (late)  
what ECG changes seen in inferior infarct   Q in II, III, and aVF (late)  
agents in acute MI tx that decrease mortality   ASA, b-blocker, ACEI  
what's Dressler's syndrome, how tx?   F, malaise, pericarditis, incrsd WBC, pleuritis wks-mos after MI; tx w ASA  
how tx acute pericarditis s/p MI   ASA (not NSAIDs or steroids or will impair scar formation)  
how differentiate systolic and diastolic dysfxn in CHF   systolic=EF<40-45% MC due to recent MI, also cardiomyopathy; diastolic usu from HTN leading to hypertrophy, also valve and restrictive cardiomyopathy ie infiltrates  
define S3 and S4   S3=rapid filling into LV (can be nml in kids); S4=atrial systole into stiff ventricle (ie diastolic dysfxn)  
signs/sympt L sided heart failure   dyspnea/orthopnea/paroxysmal nocturnal dyspnea (1-2 hrs after sleep); nocturnal cough; S3, S4; pul congestion; Kerley B lines  
signs/sympt R sided heart failure   peripheral pitting edema (pedal edema often in elderly due to vascular insuffic); nocturia, JVD; hepatomegaly/hepatojugular reflex; ascites  
what nuclear agent used in ventriculography   technetium-99 which tags RBCs  
when do hear S3 and S4 relative to other sounds   S4-S1-S2-S3  
in CHF which b-blocker is best   carvedilol > metoprolol  
when use digitalis in CHF   EF<30%, severe CHF or severe A Fib [provides sympt relief, need to check serum digoxin levels]  
signs of digoxin toxicity   N/V, PVCs, AV block, A fib, visual disturbances (yellow or green halos around objects) or disorientation  
differentiate bw cardioversion and defib, when use which   cardiovert=shock in synch w QRS, use for A fib, A flutter, VT w pulse, SVT **if during T wave can cause V Fib; defib is not insynch and used for V Fib and VT w/p pulse  
when does bradycardia become clinically signif (what bpm)? What rx used   <45bpm, can use atropine to block vagal input  
how dx 1st degree heart block   PR >0.2  
describe types of 2nd degree heart block and tx   Mobitz I (Wenkebach)=progressive prolong PR until drop a beat, no tx; Mobitz II=sudden drop beat, tx: pacemaker  
what is the pathophysiol of Mobitz II and why treat   thgt problem in His-Purkinje (v AV node for MobitzI); can progress to 3rd degree  
how identify 3rd degree heart block, what is HR   P and QRS are dissoc, overall rate 25-40bpm  
causes of DCM   MC: CAD w prior MI, but also toxic (EtOH, doxorubicin, adriamycin), myocarditis (viral, Chagas, Lyme, HIV), cocaine, etc  
how tx DCM   similar to CHF w diuretics, digoxin, ACEI, b blockers & conisder anti coag  
when might consider adding an ICD in DCM   if EF <30-35%  
causes hypertrophic cardiomyopathy   often genetic AD inheritence  
describe physiology of hypertrophic cardiomyopathy   diastolic dysfxn where can't fill ventricles, but also dynamic outflow obstruction bc assym hypertrophy of septum  
describe murmur and how it changes in hypertrophic cardiomyopathy   systolic ejection murmur that decrses w squatting or straight leg raise, incrs w Valsalva (decrsd LV size), and decrs w handgrip (incrsd SVR causes decrsd flow across AV) **also loud S4  
presentation of hypertrophic cardiomyopathy   syncope/dizziness after exercise, angina, palpitations/arrhythmias from persistent incrsd cardiac P--if not sudden death in athlete  
tx hypertrophic cardiomyopathy   all pts avoid strenous exercise, for sympt pts give b block (decrsd HR improves filling and decrs myocardial demand) [CCB if not responding to b block]  
tx of restrictive cardiomyopathy   tx underlying (often infiltrative dzs)  
common causes of myocarditis   Lyme, Cox B, Chagas, Lupus  
causes of pericarditis   infxs: Cox A, B, TB; MI (w/in 24 hr or much later (Dresslers)), collagen vascular dz, uremia, radiation  
ECG changes in pericarditis and which is **specific to pericarditis   PR depression is specific, also see in progression: diffuse ST elev that returns to nml, then T wave inversion that returns to nml  
tx pericarditis   usu self limited and resolves 2-6wks; NSAIDs for pain  
clinical findings of pericarditis   pleuritic chest pain, relieved by sitting and leaning fwd, pericardial friction rub +/- F and non productive cough  
how difft constrictive pericarditis and cardiac tamponade   in constrictive pericarditis ventricular filling suddenly halted in late diastole, see JVD w prominent x AND y descents  
unique clinical findings of constrictive pericarditis   JVD w prominent x and y descents; Kussmaul's sign: JVD doesn't decrs w inspiration  
dx and tx pericardial effusion   dx=Echo, tx=repeat Echo 1-2 wks, only pericardiocentesis if cardiac tamponade or if want to analyze fluid  
unique clinical findings of cardiac tamponade   JVD w prominent x and NO y descents; pulsus paradoxus: BP drop >10mmHg during inspiration  
describe 4 heart sounds, their order, and what mean   (S4)-S1-S2-(S3); S1=MV/TV, S2=AV/PV, S3=rapid LV filling, poor LV fxn, S4=stiff/hypertrophied ventricle  
describe murmur for MS, MR, and MVP   MS=opening snap, late dias rumble, MR=holosystolic murmur; MVP=midsys click, late sys murmur  
describe murmur AS and AR   AS=harsh systolic ejection murmur, AR=early dias murmur  
cause of MS, tx   usu RHD, tx=anti coag, diuretics for pul congestion, endocarditis prophylaxis, if severe perQ valvuloplasty  
what is progression of symptoms in AS and px   asympt for yrs then angina (3yrs avg survival), syncope (2yrs), CHF (1.5yrs)  
compare murmurs and what incrs/decrs them in HCM and MVP   both have sys murmur that incrs w standing and valsalva, decrs w squatting but handgrip will incrs murmur of MVp and decrs murmur in HCM  
describe murmur in AS and location to hear it   2nd R intercostal, cresc-decresc sys murmur radiates to carotids  
what's parvus et tardus   delayed and decreased carotid upstrokes seen in AS  
sustained PMI and precordial thrill can be seen in   AS  
at what AV area is stenosis severe   <0.8 (nml is 3-4 cm^2)  
tx AS? Timing?   valve replace in all sympt pts  
which connective tissue/rheum dzs can get AR   AV=Ehlers-Danlos, ankyl spondyl, MarfansSLE; Aortic root=Behcets, Reiters, OI  
clinical findings of AR   widened pulse P/Corrigans pulse/water hammer pulse; early dias murmur/Austin Flint murmur (BF hits MV)  
when in the dz process would LV EF start to fall in AR   very late  
how does acute MR v chronic MR present differently   in acute LA doesn't accommodate and BF into lungs causes pul edema, in chronic see pul HTN  
causes of actue and chronic MR   acute=pap rupture s/p MI; chronic=RHD, Marfans, cardiomyopathy  
tx MR   decrs afterload w vasodilators  
causes of TR   usu RV dilation, MC 2ry to LV failure (also TV endocarditis in IV drug users)  
clinical findings in TR   RV failure (incrsd JVD, ascites, hepatomegaly), pulsatile liver, v waves in JV pulse w rapid y-descent  
where listen for TR, describe murmur   LLSB, holosys murmur incrs w inspiration  
when consider TR repair/replace   if severe TR and no pul HTN (usu repair or annuloplasty, rarely replace)  
describe pathophysiol of MVP   excessive tissue from myxomatous changes, rarely MR, usu asympt  
tx MVP   usu asympt, endocarditis prophyl, surgery rarely needed  
which valves MC involved in RHD   MV, but also can include AV or TV  
name 5 major criteria for RHD   migratory polyarth, eryth marginatum, cardiac, chorea, subQ nodules  
name 6 minor criteria for RHD   h/o RF, evidence h/o strep, F, incrsd ESR, incrsd PR, polyarthralgias  
how dx RHD   if 2 major criteria or 1 major and 1 minor  
tx acute RF, how monitor progression   NSAIDs, C reactive protein monitors tx  
if P of RA, RV, PA, PCWP all incrs, what dz   MS  
if PA incrsd, PCWP nml, what dz?   pul HTN  
if RA, RV P incrsd, but PA and PCWP nml, what dz?   R heart failure  
what's the bug and pt who usu presents w acute endocarditis   Staph Aureus on nml valve in IV drug user (usu TV)  
in subacute endocarditis name bug for native valves, prosthetic   prosthetic=Staph Epi (<60d, otherwise more likely Strep); native=Strep viridans  
cxns endocarditis (or may present with these findings)   GN, pul emboli  
name Duke's major criteria for endocarditis (3)   sustained bacteremia w bug known to cause endocarditis, new valve regurg, echo showing endodamage (ie veg, abscess, valve perf, prosthetic dehisc)  
name Duke's minor criteria for endocarditis (6)   predisposition (abnml valve or risk of bacteremia), F, vascular signs (emboli, intracranial hemorr, Janeway), immune signs (Osler, GN, Roth spots, rheumatoid factor), + blood cx not meeting Major criteria, + Echo not meeting Major criteria  
how dx endocarditis using Duke's criteria   2 major OR 1 major, 3 minor OR 5 minor  
MC ASD   secondum  
key clinical exam finding ASD   wide, fixed split of S2  
when repair ASD   when Qp:Qs >1.5-2  
signs of Eisenmonger for VSD   once switched to R to L shunt get SOB, dyspnea, chest pain **cyanosis  
where listen for VSD, what hear   4th L intercostal, hear blowing holosystolic  
describe CXR findings for coarct   may see rib notching and 3 from dilation before and after coarct  
when see pul HTN w VSD? ASD?   pul HTN pretty common in VSD, occurs later (40yo) in ASD  
clinical findings PDA   wide pulse P, bounding peripheral pulse  
what PDA assoc w   congenital rubella, hi altitude, premie  
describe murmur in PDA, where hear?   continous machinery murmur, hear at L 2nd intercostal  
tx PDA   if no pul vascular dz correct, if pul HTN or R to L shunt **DON'T CORRECT  
what is cut-off for hypertensive emergency   end organ damage + BP of > 220/120 (can be either systolic or diastolic)  
what are end organ damage signs for hypertensive emergency dx   CNS: papilloedema, altered mental status/hypertensive encephalopathy, intracranial hemorr; Renal=RF or hematuria; Heart=unstable angina, MI, Ao dissection; Lungs=pul edema  
tx hypertensive emergency   reduce BP 25% in 1-2hrs,  
what tx/management paradigm for pt w severe HA and very hi BP   first lower BP, then order CT (r/o subarachnoid hemorrh), then LP  
what class of Rx are dihydropyridines? What are they used for? Name some   CCB, vasodilation (ie decrs BP), nifedipine, amlodipine [as opposed to other CCBs like verapamil, diltiazem]  
name some alpha1 adrenergic agonists used for BP   phenoxybenzamine, prazosin, terazosin  
name some direct acting vasodilators   hydralazine, minoxidil  
what are some central acting agents that lower BP, how?   methyl dopa and clonidine, both are central acting adrenergic agonists  
what are 2 types of Ao dissections, and how might they present differently   type A=proximal can have anterior chest pain and AV regurg; type B=distal can have interscapular pain  
immed tx of Ao dissection   lower BP w IV b blockers and Na nitroprusside (BP <120)  
describe MC pathophysiol and pt for abd Ao aneurysm   usu atherosclerosis (+/- trauma, HTN, smoking), in male 65-70 bw renals and iliac  
describe location atherosclerotic Ao aneurysm v syph or CT dz   syph or CT dz more often thoracic than abd  
long-term tx Ao aneurysm   type A=surgery, type B=medical management  
clinical signs of ruptured abd ao aneurysm   hypotension, abd pain, palpable abd mass--if those signs, don't do any more tests, take to emergent laporatomy  
dx abd ao aneurysm   US  
tx of unruptured abd ao aneurysm   surgery if >5cm or symptomatic  
MC locations of PVD   MC=femoral artery, also popliteal artery and aortoilliac  
signs of PVD of aortoilliac, name?   Lehriche syndrome-claudication of butt/thigh, impotence bc paralyzed L1, decrsd femoral pulse  
describe intermittent claudication   reliable reproducible pain, ie walk same distance, that completely resolves w rest  
physical exam findings PVD   decrsd pulses, decrsd hair, thickened toe nails, decrsd temp skin  
dx of PVD, cut-offs   ankle to brachial index (compares S BP of ankle to arm): nml 1 or grtr, claudication <.7, rest pain <.4  
key tx PVD, new Rx   **stop smoking!! Modify other risk factors, trental (pentoxifylline) decrs viscosity; surgery only when severe refractory pain (bypass or angioplasty)  
MC presentation, location of acute arterial occlusion   usu embolizaion in femoral artery, MV from heart, esp A fib  
tx acute arterial occlusion   immed anti coag w IV hep, emergent embolectomy using Fogarty cath [bypass if fails]  
dx of DVT   US (good to see in popliteal and femoral, less good for calf), D-dimer can use to r/o (high sensitivity, low specif)  
how to decide when to tx for DVT   is intermed/hi probab DVT and US + then anticoag, if US - then repeat US q2-3d for up to 2wks; if low/intermed probab and US - then redo US in 2d  
how anticoag for DVT   IV hep for PTT 1.5-2; start warfarin once heparin is therapeutic, once warfarin is INR 2-3 then keep heparin for another 48hrs, then d/c heparin and continue warfarin for 3-6 mos  
cause of chronic venous insuffic   usu thgt to be DVT, even if no evidence of past DVT  
pathophysiol of chronic venous insuffic   DVT destroys valves in veins, leads to ambulatory venous HTN-> edema, extravasation or RBC (pigmentation), local hypoxia (so ulcer w little trauma)  
tx of chronic venous insuffic ulcer   wet to dry dressin, unna venous boot (external compression stocking), 80% will heal, otherwise need split-thickness skin graft  
clinical presentation of superficial thrombophlebitis   pain, tenderness, errhyth, specifically coursing vein  
tx of superficial thrombophlebitis? If cellulitis also present?   just analgesic, if cellulitis need bed rest, elevation, hot compress, and Abx ONLY if suppurative drainage  
name 4 types of shock   cardiogenic, neurogenic, hypovolemic, septic  
common features to all shock   lactic acidosis, anuria/oliguria, hypotension and tachycardia, altered mental status  
cut offs for cardiogenic shock   SBP<90, UO<20 and adequate LV filling P  
describe CO, SVR, and PCWP in cardiogenic shock, what key relative to other types of shock?   CO decrsd, SVR incrsd, PCWP incrsd; only one where JVP/PCWP incrsd  
tx cardiogenic shock   dopamine, +/- dobutamine; IV fluids harmful if hi LV P, IABP can help  
how does IABP work and help   sits just distal to subclavian, deflates just before onset of systole (reduce afterload), inflating at onset of diastole (to incrs coronary perfusion); net incrs CO, coronary perfusion and decrs myocardial workload  
define difft classes/stages of hypovolemic shock and changes at each   Stage I=<20% blood loss, body compensates; stage II=<30% see incrs pulse and RR and decrsd UO; stage III=<40% those get worse then also get decrsd sys BP, confusion; Stage IV=>40%, no UO  
describe CO, SVR, and PCWP in hypovolemic shock   incrsd SVR, decrsd CO and PCWP  
describe CO, SVR, and PCWP in septic shock, what key relative to other types of shock?   dilation (decrsd SVR and PCWP) with heart trying to keep up (incrsd CO)--only one w incrsd CO  
t/f septic shock can present w hypothermia   t  
describe SIRs   if 2 or more are present: F or hypothermia, hyperventilation, tachycardia, incrsd WBC  
describe progression from SIRs to septic shock   SIRs present, then once blood cx + becomes sepsis, then once hypotension despite adequate fluid resusc=septic shock  
describe CO, SVR, and PCWP in neurogenic shock, what key relative to other types of shock?   CO ~nml, decrsd SVR (v septic shock where CO is incrsd)  
MC primary cardiac neoplasm, describe, describe key clinica exam finding   atrial myxoma, benign, pedunculated usu on septum near fossa ovalis, hear diastolic plop  
what's the cut-off for preHTN? HTNI? HTNII?   PreHTN=120-139 and 80-89; HTN I=140-159 OR 90-99; HTN II=160 OR 100; needs to be measured 2x >4wks apart w/o caffeine or smoking  
MC 2ry causes of HTN   MC=renal artery stenosis, MC in young women=OCP, also CRF, endocrine (aldosterone, steroids, Cushing), coarct of Ao and sleep apnea  
MC tx HTN   b blocker and thiazide  
Rx HTN in DM   ACEI  
before prescibe diuretic what test?   preg test in young women  
what cut-offs of HDL count as CAD risk   HDL<35 (>65 counts as negative risk)  
what's considered fam hx CAD   MI m: <55, f<65 yo  
name 3 MC familial hyperlipidemias and what's elevated in ea   Iia=fam hypercholesterol (hi LDL); Iib=combined hyperlipoprotein (hi LDL, vLDL); IV=endogen hyperlipid (hi vLDL)  
causes of 2ry hyperlipid   endocrin (hypothyr, DM, Cushing, steroid Rx, estrogen), nephrotic syn, uremia, chronic liver dz, Rx=thiazide, b blocker, HIV protease inhib  
what does EtOH do to lipid profile   incrs TG and HDL, but not overall  
how calc LDL   LDL=tchol - HDL - (TG/5) **note: can't measure LDL directly, always calculate  
what are cut-offs for lipid profiles   [tchol/LDL/TG] ideal: <200/130/125; high 240/160/250; bw those 2 is considered borderline  
what's screening for lipids   >20 screen q5 yrs (just tChol and HDL), if abnml to full fasting lipid panel, which includes TG and calc of LDL  
at what LDL do you start Rx   if CAD or no CAD and >2 risk factors: 130; if 2 risk factors: 160; if 0-1 risk: 190  
what is goal LDL for difft pt grps   if CAD=100, if 2 or more risk=130; if 0-1 risk factors=160  
at what TG start tx   >500  
dietary therapy for lipid   <30% calories from fat and <10% from sat'd fat, <300mg/d chol  
Rx for LDL   statins (atorvastatin and simvastatin are most potent)  
Rx for TG and HDL   niacin  
when use colestipol for hyperlipidemia? How change which lipids?   bile binding (colestipol, cholestyramine) only used in hi risk w statins and niacin bc bad GI SE and poorly tolerated, will decrs LDL and incrs TG  
SE statins   harmless CPK, but need to monitor LFTs (q 1mo for 3mos, then q 3-6mo)  
SE niacin   same LFT as statins, also flushing and pruritus  
what's last line for hyperlipidemia? What do to which lipids? SE?   fibrates (gemfibrozil) decrs vLDL and incrs HDL, SE mild GI, mild LFT, gynecomastia, gall stones, wgt gain, myopathies  
supraventricular tachycardias w reg QRS (4) and distinguishing features on EKG   (parox) atrial tach (abnml P, consistent), atrial flutter (saw tooth P), AVNRT (no P, reg QRS), AVRT (retro P after QRS)  
how divide arrhythmias based on QRS (3)   reg QRS (supravent tachycardias), wide QRS, irreg QRS  
causes of wide QRS (2)   supravent tachycard, VT  
how treat atrial flutter   anti coag and rate control, cardiovert like atrial fib  
pathophysiol of atrial tachycardia   ectopic pacemaker in atrium (adenosine can unmask underlying atrial activ)  
pathophysiol of AVNRT   reentry circuit in AV node, depol atria and ventricle at same time  
treatment AVNRT   carotid massage, adenosine (cardiovert if unstable)  
pathophysiol of AVRT   (AV reenatrant tachycardia bypass tract (WPW)  
treatment AVRT   same as AVNRT, carotid massage, adenosine (cardiovert if unstable)  
EKG signs of VT   3 or more PVC, AV dissoc, wide QRS w reg rhythm  
treatment VT   cardiovert + antiarrhythm (amiodorane, lidocaine, procainamide)  
causes of irreg QRS (4)   MAT (3 or more difft P), A fib (no P), V fib (EKG totally erratic), torsades de points  
causes of MAT   COPD, hypoxemia, multiple atrial foci  
treatment MAT   underlying dz (ie COPD), verapamil and b blocker to control rate and suppress foci  
causes of A fib   PIRATES=pul dz, ischemia, RHD, anemia, thyrotoxicosis, EtOH, sepsis  
when cardiovert in A fib   <48hrs and no atrial clot by TEE or >6 wk warfarin  
tx A fib   anticoag and rate control (CCB, B block, digoxin), cardiovert when nec  
tx WPW   procainamide or quinidine (not digoxin or verapamil) [yet AVRT says carotid massage, adenosine and cardiovert if nec]  
key EKG changes for K+, Ca++   hyperK=tall tented T waves, hypoK=loss T waves + U waves; QT prolong if hypoCa++; QT shorten if hyperCa++  
premature atrial complexes (PACs); look on EKG, incidence, tx   early P waves of difft morph than nml P waves; found in 50% nml adults no signif but can be precursor to isch in dzd; no tx but b blocker can help if sympt (palpitations)  
PVCs; look on EKG, incidence, tx   wide QRS w compensatory pause (p wave buried); found 50% men most pts asympt--if sympt b-blocker; freq PVC and underlying heart dz at risk SCD, consider iCD  
what's bigeminy on EKG? Trigeminy?   sinus beat followed by PVC, sinus beat followed by 2PVCs,  
what's the diff cardioversion and defib? When use which?   cardioversion=shock delivered in synchrony w QRS (don't hit t-wave or can cause V-fib), for Afib/flutter, SVT, VT w pulse; defib=not in time w QRS--use for V Fib or VT without a pulse  
what's the order of tx of Afib in hemo stable pt?   rate control (60-100, use Ca over b-blockers), cardiovert (electric prefered), anticoag (INR 2-3)  
t/f: chronic A fib w/o other signs heart dz <60 require anticoag   no  
EKG of AVNRT? AVRT?   narrow QRS, no p waves; narrow QRS w retro p waves  
how ID 1st deg block? Tx?   PR >0.2 w QRS after every p; no tx  
how ID 2nd deg block? Type I v II?   Mobitz I: progressive prolong of PR until lose a QRS; Mobitz II: sudden drop of QRS  
tx 2nd deg block?   I: no tx; II: often progress to complete heart block, need pacemaker  
how ID 3rd deg block? Tx?   no corresp bw p and QRS; need pacemaker  


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