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164 Cards in this Set
- Front
- Back
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WThat is most common sustain cardiac arrhtmia
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Atrial Fibrillation (AF)
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Does the risk of Atrial fibrillation increase with age
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YES appox 70% are between 65-85 years old
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Atrial fibrillation is about equal in men and women (slightly higher when >75, and is less prevelant in what race
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Blacks
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Atrial fibrillation is assoicated with an increased risk of
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storke, HF, and all cause mortaility especially in women
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What are triggers of AF
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sympatehtic/parasymthatic stimlaution , bradycadia,
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One of the major problems that cause AF are the presence of
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eptopic foci, which have the ability to gnerate electrical impules or wavlets
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Where are eptic foci primraily found
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along the pumonary vein
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How can we ablate the eptopic foci
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cather radioabilitation when medications have failued
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On an ECG the atrial impules discharge at rat eof >300, resulting in irregular F waves, the AV nodes can protect teh venticles so ventricular rate may be normal between 60-100, or the venticular rate may exceed
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120 bpm--which is dangerous
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Atrial Fibrillation demonstate 1 of 3 clinic patterns
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Paroxysmal
Persistent Permenant |
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What is paroxysmal AF
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self-terminating epidose <7 days but usualy less <24hrs
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What is persisten AF
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NON-self terminations epidoses last >7 days
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What is permenant AF
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long epidose > 7 days with failed cardioversion or where cardiovesion is not possible
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What is Lone AF
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person without structural or cardiac/pulmonary disease with a low risk for thromboemolism
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Lone AF is typically applied to patients younger than
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60 years
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Pts who have AF have variable clinical presenation many are asymptomic or complain of
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SOB, palpitations or fatigue
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Some pts with AF also experience Chest ptain, espically when
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ventrciular rate in not controlled regarless if they have CAD
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Sustain AF with rapaid ventricular response may lead to
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tachycardia-mediated cardiomyopathoy
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Syncope is rare in patients without
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other cardiovascular condictions such as sinus node dysfuction or aortic stenosis
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What are goals when treating pts with AF
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prevetion of stroke (thromboemolism, prevnetion of tachcardia induced cardiomyotahtoy and symptom relief
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AF is a loss of organized atrial contraction that can lead to
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stagnation of blood espically in the left atrial appendage resulting in trhombus formationa and embolism
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May AF be assoicated with a hyeprcoaguable state
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YES
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Is Stroke the most common thromboembolitic event in AF
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YES
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Initally all pts that present ot emergency room with AF will be acutely treated with
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anticouagulant
Heparin or LMWH |
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What is the current standard of therapy for preventing thomboemolisim in patietns at high righ for stoke
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warfarin--no MATTER WHAT
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Untreated AF often is assoicated with
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rapid ventricular ate >120 bpmp
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Ventciular dsyfuction can ocur as soon as 24hrs and contineut odeterior for 3-5 weeks, recovery of ventricular function with cessation of pacing starts within
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48hrs and normalization within 1-2 weeks
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Control of ventrcilar ate should be undertake early to prevent
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tachcardia induced cardiomyopathoy--LVD
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If pts have already developed tachdarid induced dysfuction, the immediate goal is to
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reverese the process with agreesive rate control or cardioversion to normal sinus rhythm
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Symptoms of AF can be controlled with either
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rate contrl or rhythm control strategy in older pts
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In younger pts or pts who have paroxysmal AF may require what class of drugs to feel better
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sinus rhythm to feel better
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When a rate control stragey is selected it is imporatnt to allow
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adequate time for symtpoms to improve b/c many pateitns take several motnsh for good symtpoms releift after achieving rate control
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Control of symptoms rather than elimiantion may be an acceptable goal
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YES
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An inital evulation of AF should inclue clinical history regardting the time of onset/nature of symptosm, and attention shouldbe direct to identify
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a possible rpecidtaing event that led to AF
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Symtpoms suggestive of complications should also be a part of the history they include
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heart failure and stroke
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Inital labs testing should inlcude
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CBC, metabolic panel, renal and throid functions
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Why should thyroid functions be evaluated
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as hyperthroidism can cuase AF
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What does of Echocardiogram is indicated in most patients to identify cuasatinve factors for AF
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2-D
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After the inital evulation, the 2nd part is directed at
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hemodynamic stability of patients
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What pts with AF may suffer severe hemodynamic compromise
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pts with rapid ventricular rates
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What are pts what may suffer hemodyanmic instability
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hypertropic cardiomyopathy, diastolic dyfuction, and severe mitral stenosis, or MI , PE
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Pts with life theatengin hemodtanmic compromise need to be consider for
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emergent cardioversion without consideration to anticoagulation status
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Once hemodyanmic status is addresses what is evaluated
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potential preciptaitng events
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What are cardiac disorders that may underlie AF
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percardiditis, HF, thoracic surgery, or Wollf-Parksinon-White syndrome, mitral stensis
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What are NON-cadraic condiations that can precipaitate AF
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penumonia, PE hypoix, thrytoxicosis, and bindge drinking
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Regarding ot the potential precipitating events what should be initated in all pts
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antigcouaglation b/c could be causative or coincidinal--out brought out your underlying condition
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What are the 2 thereapteic options to control symtoms in AF
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rhythm control or rate control
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What does rhythm control do
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sinus rhythm is re-establish
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What does rate control do
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pt reamin in AF with control of ventricular rates
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What is cardioversion
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the method used to convert a patient from AF to normal sinus rhythm (mainly rhythm control)
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What are 2 types of cardioversions
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1. Direcute current cardioversion
2. Pharmacological cardioversion |
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What is Direct current cardioversion
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electical shock, which is applied to the heart to shock it back into normal sinus rhythm
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Cardioversion should be consider for 2 pt populations
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1. symptomatic AF
2. Those present with AF for the 1st time |
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Symptoms of AF can ragne from severely decompnested heart faulre to hypotensino or angins, regarldess of the DEGREE of severity ANY symtpoms warrant consideration of
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carivresion
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What is a resonable goal in pts who have a 1st tiem diagnosis of AF reglarless of symtoms (unless some indication that it has been present for many years)
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restoration of sinus rhythm
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What is the purpose of cardioversion in pts who are asymptomic or newly diagnosed
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is to slow the progession of AF, is it a progressive disease
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Maintain sinus rhythm is unlikely to have a meaningul clinical impac on
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older pts who ar asymptomic
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Cardioversion is NOT applied to pts who ahve PERMANT AF, however ALL pts should receive
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anticoagulation or antiplateletn therapy
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What is another pt population that may benefit from cardioversion
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those with postopertive AF--b/c anticoagulation is undesirable
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When would postoperative pts be cardioverted
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within 48hrs of AF in order to avoid anticoagulation
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Are pharamcologic and electrical cardioversion more likely to succeed in pts who have episodes of shorter duration
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YES
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AF resutls in mechaical statis of the atria and they are at risk for developing thormbi and embolization, which is this risk really high
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around the time of cardioversion
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Why is the risk highest for thormbi during cardioversion
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1. recovery of atrial contration post cardioversion may cause fragmentation and embolization of preexisting thrombosis
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Recovery of atrial contraction post cardioversoin may cause
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fragmentation and embolization of preexiting thrombus
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The recovery of atrila mechianical fuction can lag behind electrical function, up to 4 weeks, what happens after atrial mechianial stunning
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lead to a clot--thus risk for a clost may endure for serveral week post cardioversion
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Why is anticoagulation given before cardioversion
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b/c cardioversion can induce a clot
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What are the 2 goals of anticouaglation pre-cardioversion
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minize the likehood of an unstable thrombus and prevent formation
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To minimizes the likelihood of an unstable thrombus being present at hte time of cadrioversion ONE or two strategies must be used
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Either
Empiric Anticoagulation Short-Term Stategy |
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When should empiric anticoagulation be iniated PRIOR to cardioversion
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3 weeks PRIOR
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How long does an unstable thrombus take to organize and adhere to the atrial wall
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2 weeks
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Under the Empiric Strategy pts should be treat with either
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Warfarin or Enoxaprin or dalteparin daily prior to cadrioversion
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Warfarin INR goal is 2.5 (2-3) (MUST CHECK INR weekly) what is enoxaprin and dalteparin dosing
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enoxarin 1mg/kg BID
dalteparin 200 Units/Kg qd |
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What pateitns are candidates for SHORT-TERM anticoagulation with transesopheageal echocadriorapy TEE
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pts that do not have a pre-existing thormbus on a TEE
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What are antigocaulants used in short term strategy
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Heparin or LMWH BOTH followed by TEE
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If not thrombus is seen on the TTE then what
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cardioversion is preformed
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IF a thormbus is found on the TEE than
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the empiric anticoagulatino stragegy is employed
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The choice bettwen the empric or srhot-term anticoagulation straget is dependent upon the
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urgency of the situation (if pt is exremeyl symtpomtaic or uncomformatble
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What is dosing of Heparins
Enoxparin and dalteparin prior to TEE |
Heparin 60U/kg bolus, then 12 units/kg/hr
Daleparin 200u/kg qd Enoxaprin 1mg/kg BID |
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Once cadrioversion is complete then the pt should be anticoauglation with
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warfarin at an INR of 2-3 for 4 weeks
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Why should pts undergo at least 4 weeks of therapuetic anticouagltion post cadriversion
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b/c of the dealy of up to 4 weeks of atiral MECHICAL fuction post cardioconversion
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Most thromboembolitc events occur within
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the 1st few days post cardioversion
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When should overlaapign thearpy with UFH or LMWH be adminsteted post cardioversion
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if the INR is <2
need LMWH or UFH+warfarin |
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For AF lasting <48hrs the likelihood of thormbus formation and embolizaiton is
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LOW==SO anticoagulation is NOT routeinly recomment
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ANticoaugltion is NOT recommented in pts with AF <
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<48hrs
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Is Pre/Post cardioversion recommended for short term duration episodes
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NO
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What is the only way you can determine the TRUE onset of AF
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12 lead ECH
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Are symptoms unreilable as a marker of presence or absence of AF
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YES---
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In the absence of ECG evidence for true onset of AF, what must we ASSUME
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that the episode have been going on for more than 48hrs
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Most pts who require cardioconversion undergo
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DIRECT electrical cardioversion
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Does direct electrical cardioversion have a higer success rate
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YES
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If pts undergo electrical cardioversion, must also be admistnered some form of
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sediation as general anestehisia or agents such as midazolam, fentanyl or proppofol
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What electrolytes must be within speicifc limits PRIOR to electric cardioversion
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Pts K+ and magnesium
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WHat are goals ranges for K+
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4.5-5.0
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What are the magnesium goals
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1.5-2.1
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Can excessive current deliery lead to mycardial damage
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YES
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If a pts fail exteneral electrical cardioversion, what can be attemeted
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internal catherther cardioversion can be attempted
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When is only time phramacolgical cardioversion is considered
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1. short-druation AF in highly symptomatic pts w/ little or NO sturcutral heart disease
2. as adjust to electical |
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Why would pharmacolgoical be used as adjust thearpt to electrical cardioversion
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in pts who have failed pervious electrical cardioversion
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If a pts AF has persised for >48hrs what must be iniated
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anticoagulation therapy must be iniated on emerical or short term
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What must be adminstered PRIOR to ANY antiarryhtmic medication
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anticoagulatnt
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Phramacolgical cardioversion is given acutely and continued for several months,
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YES
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THere is NO set time period to stop antiarrhytmic medications, however is pts go back inAF following pharamacolgical cardioversoin they may
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remain on antiarrhtmic medications life-long
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When pharmacolgic cardioversion is used, the pt is admitted into the hospital for
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a MINIMUM of 3-4 days
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Should Mg and K+ always be within specific ranges PRIOR to adminstition of any anti-arythmic
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YES
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EKG will be used at besline and again before and after each dose of anti-arrythmic agnet
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YES
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Election of ayntiarrhmtic agents should be direct by a
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saftey based appraoch based on comorbid conditions
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What are Class Ic agents
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Flecaininde, and propafernone
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Felecaninde and profapernone are CONTRAINDICTED IN
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Ichemic heart disease (MI) b/c increase mortatilty
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What are the inital choice of AF with struurally normal Hearts (no ischemic heart disease)
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Flecainide, propafenone, or sotalol
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What classes of drug prolong cardiac repolraization and be assoicated with TOrsades de pointes
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Class III (sotaol/dofetedlie)
Class Ia (PDQ) |
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Many patients at risk for TOrsades can be identifed by monitoring, however late episodes can occur in the setting of
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hypokalemia, bradycardia, or rendal dysfuction
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DoesAmidoraone have a very low risk for causing TOrsades
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YES
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Amidarone is MOST effective anti-arrhtmic drug, however
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has many organ toxicity such as thyroid, pulmory and nuerolic, hepatic, and dematgolic that limit its usefulness
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What is the perfered inital therapy for Left ventricular hypertrophy
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amiodarone
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What are the perferred agents for HF
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amidarone/dofetelide
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Pts with Ischemic heart disease should NOT be given
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flecaindie/profafenone
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Pts with ISchemic Heart disease of CAD should be given
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Sotalol or dofetilide
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Sotalol and dofetelide are should be avoided in pts
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signifiangt renal dysfuction b/c they are reanlly excreted, and complex medical regimens, if changes in electrolytes could occur
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If drug therapy fails then what is consider
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catheter ablation of the eptoic foci can be consdier
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What is oral dosing of Amiodarone
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inpatient: 1.2-1.8 g per day in divided dose until 10g total, then 200mg qd mainence
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What is IV doing of Amiodarone
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5-7mg/kg over 30-60minutes then 1.2-1.8 per day continous IV or oral, til 10g total, then 200 mg maitaine
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When in amiodarone a perferred agent for arrthmias
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Left ventricular hypertrophy, HF (LVD)
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What is a major adverse effect of amiodarone
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hypotension, bradycardia consitiaption, GI upset,
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What is required monitoring for amiodarone upon initation
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throid, liver panels, and chest radiography
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Pts on amiodarone should undergo mointing every 6 months and ahve
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pulomary function tests for Carbon monoixde
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Amiodarone pulmonary toxicity correlated most cloest with
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culumlative dose receive and is rare in pts receivng 200mg qd
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When is amiodarone onset of Action
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8-24hours
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Class IC show a more rapid onset of action, as soon as
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1-2 hours after administraion
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Amiodarone interacts with what drugs
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wafarin, digoxin and cyclosporine
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What class of drugs is Procainamide
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Class IA
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What is oral dosing of Propafenone
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600mg
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When should procainamide be terminated
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hypotension or QRS cokplex prolongation by >50%--PROCANAMIDE can prolong QT interval and lead to rpoarrhtmia
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Procainamides negative inotropic effects and vasdilation limit its use, what is it metabolite
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NAPA (N-acetylprocainamide)
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Monitoring of NAPA is procainamide is recocmmned in pts who have
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renal dysfunction
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Procainamide is the drug of CHOICE in what patients
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WOlf-Parkinson-White syndrome
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What are other side effects of prcainamide beside hypotension/QT prolongation
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bone marrow suppresision, Coomb's, juandice, and lupus-like symptoms
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What drug class is Ibutilide
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Class III
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What is dosing of Ibutilide
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1mg is given as an infusion over 10minutes and be repated 10-20 minutes later if AF persists
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Class III agents can cause Torsades de Pointes, however Ibutilide causing Torsades is limited to pts who have
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LVD or porlongation of QT intervail, especiall in presence of hypokalemia or hypomagensaemi
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Ibtuiltides should not be adminsiteed in pts with Left ventricular ejection fraction <, or a correct QTC >
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EF < 35%
QTC >460 milliseconds |
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Main SEs of Ibutilide
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Torsades
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Dofetilide is a NEWER Class III ORAL anytarrhtmic agents, what limits its USEin teh ACUTE setting
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it may take days to weeks before cardioversion
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Dofetilide dosing is based on
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CrCl
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Dofetidle dose with CrCl
>60 40-60 20-40 <20 |
>60 500 mcg BID
40-60 250 mcg BID 20-40 125 mcg BID <20 contraindicated |
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Dofetilide is renally excteted is contraindicated in combination with
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HCTV PKM
Cimetide HCTZ, ketoconazole, megestrol prochlorperzine, thrimehtoprim, verapamil |
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When is rate control given is preference
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in less symptomatic elderly pts, or noncompliant pts
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Rate control may be preferred as rhythm control may warrant a higher need for hospital admissions for
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drug initations and tirations
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What are drugs used to control rate
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Beta blockers
Ca+ channel block DIgoxin |
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Rate control drugs only control ventricular rate
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YES
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Where are beta blockers most likely effective in
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postoperative pts who have high adrenergic tone
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What is dosing of Metoprol
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2.5 -5mg IV over 2-5 minutes,
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Mteoprol can be repeated up to
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3 times every 5-10 minutes as long as hyotehions does nto ocur
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Once adeuate rate control is achieced with metorprolol (usually within a few minutes) then
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pts may be transistion to oral doses
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What is benefit of Esmolol
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in pts who are at risk for hemodynamic instaibilty
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In pts who cannont take beta-blockers or are insufficent, to control ventciular rate what may be administered
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diltiazem or verapamil
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What is dosing of ditizem
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.25mg/kg IV bolus over 2 minutes following by 5-10mg/hr
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What is dosing of verapamil
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0.075 to 0.15 mg/kg IV over 2 minutes
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Digoxin may be useful in pts with
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HF or those who have marginal blood pressure
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Dosing of Digoxin
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Loaded 0.25mg IV/Oral every 6 hours for 4 doses, then .125-.250 mg qd
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Digoxin serum concentration control rate should be beween 0.5-2, unless HF, then is
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0.5-0.8
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Can Amiodarone also be used for rate control, and onset
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cuasing slowing of rapid ventrciular ate within the 1st hour after adminstration--other propertes begin later
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Beta blcoker and non-dyrhydropyridine Ca+ channel blockers shoud be avoided in pts with
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pulmonary edema and LVD
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Shoud an antigcoagulant be give prior to rate control
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YES
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Rate contols onset of action is must slower than rhythm, what drug should be avoided if thrombus is present
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amiodarone as rate contorl
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