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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
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
Created by: ehstephns
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When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

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