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54 Cards in this Set
- Front
- Back
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sVT ECG
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narrow complex - tach- qrs <120 ms
except with coexisting BBB- QRS will remain wide rate related abberancy- at fast HR - QRS can go wide with BBB Preexcited- by accessory pathway from A to V- a way to bypass AV node- - will activate V more slowly- QRS is wide if not sure treat as VT p waves after QRS |
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SVT defn
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does not originate in ventricles
usually paroxysmal- can be persistent - tachycardia- -benign- req tx for symptomatic relief- or to prevent tach induced CM- persistently elevated HR can lead to HF and LV dysfunction 1in 500- 1000 |
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symptoms SVT
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variable
asymptomatic palpitations/ heart racing/chest pain, discomfort/dyspnea/presyncope usually sudden onset and offset vs Sinus tach is more gradual |
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SVT common entities
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atrial tach-
av node re-entry tach av re-entry tach- bypass tract junctional tach- post pediatric ohs afib, afl, multifocal atrial tach, sinus tach- separated from SVT |
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reasons you can acquire SVT
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DUAL AV node physiology- 2 functional pathway to AV node- that can set up re-entry
accessory pathways- connecting A to V anatomic obstacles- scars |
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AVNRT
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AV node re-entry tach
dual AV node physiology fast pathway- conducts rapidly with long refractory period slow pathway- conducts slowly- shorter refractory period- can conduct two one after the other mos common SVT >60% - patient has ectopic beat - dont notice it- may start to conduct down fast pathway but due to longer refractory period, doesnt conduct.- blocks here conducts slowly down slow pathway- but makes it down due to shorter refractory period by the time the impulse reaches turn around point- fast pathway has recovered, can get a re-entry circuit all contained in AV node |
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AVRT
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atrio ventricular re-entry tach
AV node is part of circuit as well as accessory pathway is orthodromic- AVRT- impuslse goes down accessory pathway- gives a wide QRS (not using fast HIs) then goes backwards, up the av node to atrium orthodromic - QRS will be narrow antidromic - QRS will be wide - preexcited wolf parkinsosn white pattern |
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wolf parkinsosn white pattern
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have ventrcular pre-excitation on ECG+ symptoms of palpitations
on ECG: short PR interval, QRS widening onset of QRS is slurred - usually indicates accessory pathway |
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atrial tach
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least common SVT
localized to atrium - no av node or ventricles see SVT- trasient AV block- not AVRT or AVNRT- usually ATach may be irregular at beginning: automatic focus- area of cells with inc automaticity micro-rentry macro rentry |
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SVT evaluation
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stable vs unstable
unstable : synchronized- cardioversion 12 lead ECG hx: WPW, Epstein's (accessory pathways) HF, transplant, surgeries other med conditions: asthma, COPD, CVA MI |
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SVT ECG analysis
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look at relationship of QRS complexes and P waves
1:1 ratio- one p wave fro every QRS more P waves than QRS- atrial tach no obvious P waves- good sign that p waves are buried on top of QRS. compared sinus rhythm ECG to ECG in tach- and look for subtle changes in QRS- implying P wave superimposition- this is usually AVNRT - activates Atria and V at the same time AVRT- need time to go from atria to V back to A- so p waves will be outside QRS |
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PR interval
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what is the relationship of p wave to the QRS
does it come close to the QRS before- short RP or does the P wave fall close to the next QRS- long RP short RP- AVNRT- AVRT long RP - - AT |
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SVT acute diagnostic and tx manoevers
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to confirm diagnosis
valsalva , vagal manoevers, adenosine - hyperpolarize cells in AV node- causes temp AV block all affect AV node conduction if tachycardia stops with AV node block- then know AV node is involved - AVNRT or AVRT do AV block - with ongoing rapid activity - know AV node is not imp atrial tach |
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how to look for SVT if no recorded tach
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holter monitor - 24- 48 hours
event recorder: loop recorder - push a buttom when experiencing symptoms non looping- also just push a button |
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tx of SVT
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mainy b/c of symptoms
Prognosis can be altered in tx: WPW tach induced CM for symptoms: conservative tx- vagal manoevers- adhoc tx medical therapy = bb, nondihydropyridine CC B_ to block AV node curative tx; with catheter ablation |
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pre-excited Afib caused by WPW
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in patients with WBW- sometimes the accessory pathway can conduct rapidly- can induce Vfib -
irregularly irregular wide complex tach - pre-excited a fib |
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ventricular pre-excitation does convey small risk of sudden death
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secondary to a fib that goes rapidly over accessory pathway with a short refractory pathway that can cause VT
symptomatic patients: syncope, young age, other markers of high risk: multiple pathways, pre-excited AF beats >240 bpm structural heart disease |
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tachycardia induced CM
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incessant tach
not usually symptomatic from arrhythmia can lead to HF and death reversible to with adequate rate control |
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what requires definitive tx
and waht are tx options |
pre-excited AF with rapid ventricular response or WPW with sudden syncope or TCM
catheter ablation adequate rate control for TCM no good therapy for preexcited AF outside of procainamide tx |
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general tx of SVT
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AV node blocking agents- bb blocks, NHP CCB, may make tachycardia less fast
and can slow ventricular response to AT catheter ablation good first line therapy or 2nd line after meds generally avoid class IC or Class III drugs; potential for toxicty and side effects |
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catheter ablation
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both diagnostic and tx
go through femoral vein - put in catheter- record electrical signals ablate tissue |
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A fib
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presentation variable
can be asymptomatic palpitations, SOB, dec exercise capacity, chest discomfort, fatigue, decreased exercise capacity HF symptoms exacerbated intercurrent illness (thyrotoxicosis) stroke/systemic embolism |
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Afib ECG
what does it increase with |
irregularly irregular ventricular response and chaotic atrial activity
common arrhythmia increases with Age, structural heart disease, HTN, medical comorbidities |
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bacground
what is AFib underlying mech |
Afib not the same in all patient
some AFib is triggered- often by bursts in pulmonary veins some AF related to abn hearts, structural heart disease, HTN, mitral valve disease, HTN, LVH |
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scope of problem of AFib
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2 million people in uS
10% over 80 |
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electrophysiological abn that predispose to AFib
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atrial ectopy- triggers usaully from pulmonary veins
structural remodelling- scars - wavefront hits areas of slow and fast conduction AF begets AF: AF alters atrial myocardial refractory period- makes AF more likely to sustain structural changes seen like dilatation can be familial- chanellopathies - first degree relative double chance of you getting one |
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clinical patterns of AFib
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paroxysmal
self terminating episdoes <1 week persistent longer than week, may not stop on their own permanent persistent for more than a year refractory to cardioversion/ give up |
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higher mortality rates in Afib patiets vs those that dont have AFib maintenance of sinus rhythm can alter this risk
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major management issues:
cant alter mortality but can lower risk for stroke throboembolism formation symptom control prevent tCM |
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Afib investigations
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hx and px
contributing/percipitating factors intercurrent illness, alcohol, HD, HTN ECG: rate/rhythm, LVH, LAE, prior MI bood: thyroid, electrolytes, cbc kidney echo - heart disease or not |
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major management issues in Afib
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thromboembolism prevention for stroke
long term strategy: pericardioversion- special circumstance- duration of AFib- more than 48 hours, give anticoagulation essentially ASA or systemic anticoagulants- warfarin |
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risk of stroke
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valvular heart disease
mitral valve probles HCM- high risk |
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CHAD score
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used for non-valvular AF
CHADS2 - point for HF, HTN age> 75, prior stroke, embolus: higher the score- higher the risk of stroke |
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anticoagulation for AFib
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aspirin vs placebo
reduce 22% warfarin vs placebo 60s%- but inc risk of intracranial bleeding warfarinvs aspirin: 36% dec in stroke, 2.1 fold of IC bleeding dabigatran vs warfarin: 35% risk dec these drugs not safe for mech heart valves |
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rhythm vs rate control
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no mortality data or stroke risk advantage for either
recurrent AF- rate control drugs less toxic- less side-effects highly symptomatic despite rate control- or limited by bradycardia- rhythm control strategy preferred |
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favoring rate control
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do better and feel better
rhythm control diffucult- structural disease |
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favoring rhythm control
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symtomatic
fail rhythm control likely to maintainrhythm- no structural issues |
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rate control drugs
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Av node blockers- BB, non-DP CCB (verapamil, diltiazam), digoxin
aiming for resting HR <80 avg HR <100 no HR >110% of max age predicted |
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rate control other methods
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pacemaker
AV node ablation and pacemaker dependent |
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asymptomatic persistently elevated HR can lead to
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TCM
tachycardia induced myopathy |
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rhythm control strategy
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antiarrhythmic drugs first line
catheter ablation for drug failure possible surgical ablation if undergoing OHS anyway |
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choice of management depends on
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LVEF low- dont use class I C
age - kidney function in older, young, long term exposure in amioderone- fat storage diuretics- hypokalemia gender - females more likely to have proarrhythmia - (any rhythm control drug has potential to produce worse rhythm) |
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rhythm control drugs
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structurally normal hearts;
go for Class I c agent first - coadminister with AV node blocker sotalol amioderone |
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Class I c agent first
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-for rhytm control- slow conduction in AV node - Na channel blockers
eg Flecanide and propafenone q |
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sotalol
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Class III- K channel blocker- prolongs repol-
caution can cause QT prolongation- torsades sycnope can point toward torsades dont use on elderly women on diuretics - hypok |
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amioderone
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CLass III BB and I
second line - most effective of maintaining sinus rhythm but adverse effects LV systolic dysfunction: use amioderone |
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LV systolic dysfunction what drug to use
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amioderone
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CAD with preserved LVEF what drug to use
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sotalol amioderone
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symptomatic control - ablation
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catheter ablation for 2nd line therapy for symptomatic drug refractory AF
predominantly left atrial procedure paroxysmal pattern- electrically isolate pulmonary veins persistent - extensive ablation |
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rhythm control
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used for symtoms only
not shown to alter stroke ris |
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atrial flutter
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organized atrial macrore-entry
same stroke risk as a fib- anticoagulate more difficult to rate control |
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ECG atrial flutter
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typical:
300 bpm saw tooth pattern in inferior leads usually no prior extensive scarring or prior surgery |
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typical AFLutter
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straightfoward to tx with ablation
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atypical flutter
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more extensive ablation greater risk
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atrial fib and atrial flutter can coexits T or F
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T
imp for coagulation issues |
