ACLS Study Guide - Florida Training Academy

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ACLS Study GuideThis purpose of this study guide is to assist you in successfully completingthe AHA ACLS course. It includes sections on: ECG Rhythm Interpretation ACLS Drugs ACLS Algorithms

ECG Rhythm InterpretationElectrical Conduction System SA Node. Primary pacemaker. Rate 60-100 The impulse travels through the Intraatrial Pathways to innervatethe atria The impulse reaches the AV Node where electrical activity is delayedto allow for more complete filling of ventricles. AV Junction is comprised of the AV Node and the Bundle of His.Secondary pacemaker. Rate 40-60 The impulse then travels into the Right and Left Bundle branches.Conducts electrical activity from Bundle of His to Purkinje Network. The Purkinje Network are fibers that spread throughout theventricles, that carry impulses directly to ventricular muscle cells. Ourlast pacemaker site. Rate 20-40

P wave:PRI:QRS:T wave: Represents Atrial depolarization Represents the time it takes the impulse to travel from the SA Node through theintraatrial pathways in atria to the AV junction and the delay at the AV node. Interval from start of P wave to start of QRS, measures 0.12-0.20 sec Represents conduction of impulse from Bundle of His through the ventricularmuscle. Represents ventricular depolarization. Should measure less than 0.12 sec Follows ST segment. Slightly rounded, positive deflection Represents ventricular repolarization, “resting phase “of cardiac cycleAbsolute Refractory Period: No outside stimulus can cause cells to depolarization From beginning of the QRS complex to the middle of the T waveRelative Refractory Period: A dangerous period. A strong outside stimulus can initiatedepolarization of the only partially recharged cells. Possibly causing alethal arrhythmia From the middle of the T wave to its end

5 Steps for Analyzing a Strip:Heart Rate:Bradycardia 60, Normal 60-100, Tachycardia 100 Count the # of R waves in a 6 second rhythm strip, then multiply by 10 Find an R wave that lands on a bold line. Count the # of large boxes to the next Rwave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3boxes - 100, 4 boxes - 75, 5 boxes – 60 Divide 300 by the number of large boxes separating the R wavesHeart Rhythm: Look at the R – R distances, are they regular or irregularP Wave: Are there P waves? Do the P waves all look alike? Do the P waves occur at a regular rate? Is there one P wave before each QRSPR Interval: Is the PRI between 0.12-0.20? Is it consistent across the strip? If it varies is there a pattern?QRS Complex: Do all of the QRS Complexes look alike? Are they regular? Is the duration 0.04 – 0.12

Normal Sinus RhythmThis rhythm represents the normal state with the SA node functioningas the lead pacer with normal conduction through the heart.Theintervals should all be consistent and within normal ranges.Looking at the ECG you'll see that: Rhythm - Regular Rate - (60-100 bpm) QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal ( 5 small squares. Anything above andthis would be 1st degree block) Indicates that the electrical signal is generated by the sinus nodeand travelling in a normal fashion in the heart.

Sinus BradycardiaThe sinus beats are slower than 60 BPM. The origin may be in theSA node or in an atrial pacemaker. This rhythm can be caused byvagal stimulation leading to nodal slowing, or by medicines such asbeta blockers, and is normally found in some well-conditionedathletes. The QRS complex, and the PR interval may slightly widenas the rhythm slows below 60 BPM. However, they will not widenpast the upper threshold of the normal range for that interval. Forexample, the PR interval may widen, but is should not widen overthe upper of 0.20 secondsLooking at the ECG you'll see that: Rhythm - Regular Rate - less than 60 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal Usually benign and often caused by patients on beta blockers

Sinus TachycardiaIt is an excessive heart rate above 100 beats per minute (BPM)which originates from the SA node. Causes include stress, fright,pain, dehydration, and exercise. Not usually a surprise if it istriggered in response to regulatory changes (e.g. shock).Looking at the ECG you'll see that: Rhythm - Regular Rate – Usually between 100 – 150 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal The impulse generating the heart beats are normal, but they areoccurring at a faster pace than normal. Seen during exercise

Atrial FlutterA single irritable focus in the atria fires in a rapid repetitive fashion ata rate of 150 – 350 beats/min. The F waves appear in a saw toothedpattern such as those in this ECG. The QRS rate is usually regular andthe complexes appear at some multiple of the P-P interval.Looking at the ECG you'll see that: Rhythm – Usually regular Rate – Usually fast 110-150 beats per minute QRS Duration - Usually normal P Wave - Replaced with multiple F (flutter) waves, usually at aratio of 2:1 (2F - 1QRS) but sometimes 3:1 P Wave rate - 300 beats per minute P-R Interval - Not measurable

Atrial FibrillationAtrial fibrillation is the chaotic firing of numerous atrial pacemaker cellsin a totally haphazard fashion.The result is that there are dhaphazardly in an irregularly irregular pattern. The ventricular rate isguided by occasional activation from one of the pacemaking sources.Because the ventricles are not paced by anyone site, the intervals arecompletely random.Looking at the ECG you'll see that: Rhythm - Irregularly irregular Rate - usually 100-160 beats per minute but slower if onmedication QRS Duration - Usually normal P Wave - Not distinguishable as the atria are firing off all over P-R Interval - Not measurable The atria fire electrical impulses in an irregular fashion causingirregular heart rhythm

Supraventricular Tachycardia (Narrow complex Tachycardia)(SVT)SVT is a narrow complex tachycardia originating above the ventricles.SVT can occur in all age groups.Looking at the ECG you'll see that: Rhythm - Regular Rate - 150 beats per minute QRS Duration - Usually normal P Wave - Often buried in preceding T wave P-R Interval - Depends on site of supraventricular pacemaker

1st Degree AV Block1st Degree AV block is caused by a conduction delay through the AVnode but all electrical signals reach the ventricles. This rarely causesany problems by itself and often trained athletes can be seen to haveit. The normal P-R interval is between 0.12s to 0.20s in length, or 3-5small squares on the ECG.Looking at the ECG you'll see that: Rhythm - Regular Rate - Normal QRS Duration - Normal P Wave - Ratio 1:1 P Wave rate - Normal P-R Interval - Prolonged ( 5 small squares)

2nd Degree Block Type 1 (Wenckebach)Mobitz Type I is also know as Wenckebach (pronounced WEEN-keybock).period.It is caused by a diseased AV node with a long refractoryThe result is that the PR interval lengthens betweensuccessive beats due to increasing delayed conduction through the AVjunction until a beat is dropped. At that point, the cycle starts again.Looking at the ECG you'll see that: Rhythm - Regularly irregular Rate - Normal or Slow QRS Duration - Normal P Wave - Ratio 1:1 for 2,3 or 4 cycles then 1:0. P Wave rate - Normal but faster than QRS rate P-R Interval - Progressive lengthening of P-R interval until a QRScomplex is dropped

2nd Degree Block Type 2In 2nd degree Type 2, the impulse either passes through the AVjunction normally or it is blocked completely.It is an all or nothingtype of thing. Beats are intermittently nonconducted and QRScomplexes dropped, usually in a repeating cycle of every 3rd (3:1block) or 4th (4:1 block) P waveLooking at the ECG you'll see that: Rhythm - Regular Rate - Normal or Slow QRS Duration - Prolonged P Wave - Ratio 2:1, 3:1 P Wave rate - Normal but faster than QRS rate P-R Interval - Normal or prolonged but constant

3rd Degree Block3rd degree block or complete heart block occurs when the impulsetravels through the atria normally but is blocked completely at thejunction.The atria and ventricles are firing separately – each to itsown drummer, so to speak.normal or tachycardic.The atrial rhythm can be bradycardic,The escape beat can be junctional (normalQRS) or ventricular (wide QRS).Looking at the ECG you'll see that: Rhythm - Regular Rate - Slow QRS Duration – Usually wide, but if ventricular impulse isgenerated low in the junction it could be normal. P Wave - Unrelated P Wave rate - Normal but faster than QRS rate P-R Interval - Variation

Differentiation of Second- andThird-Degree AV BlocksMore P’s than QRSsyesyesPR fixed?2nd degreeMobitz type IInoQRS alikeand regular?yes3rd degree AV block2nd degree Mobitz type InoWenckebach

Wide Complex Tachycardia (usually monomorphic ventriculartachycardia) AbnormalVentricular tachycardia is simply the presence of three or more ectopicventricular complexes in a row with a rate above 100. Originates fromone irritable focus so the rhythm is regular.Poor cardiac output isusually associated with this rhythmLooking at the ECG you'll see that: Rhythm - Regular Rate – Fast usually 180-190 Beats per minute QRS Duration - Prolonged P Wave - Not seen Results from abnormal tissues in the ventricles generating arapid and irregular heart rhythm.

Polymorphic V-Tach (Torsades de Pointes) Similar to ventricular tachycardia Morphology of QRS complexes shows variations in width andshape Resembles a turning about or twisting motion along base line May result from hypokalemia, hypomagnesemia, tricyclicantidepressant drug overdose, the use of antidysrhythmic drugs,or combination of these Seen in alcoholics, eating disorders and the debilitated patients

Ventricular Fibrillation (VF)Disorganized electrical signals cause the ventricles to quiver instead ofcontract in a rhythmic fashion. A patient will be unconscious as there isno cardiac output and blood is not pumped to the brain. Immediatetreatment by defibrillation is indicated. This condition may occurduring or after a myocardial infarct.Looking at the ECG you'll see that: Rhythm - Irregular Rate - 300 , disorganized QRS Duration - Not recognizable P Wave - Not seen This patient needs to be defibrillated!! QUICKLY

Pulseless Electrical Activity (PEA)PEA occurs when any heart rhythm (other than V-Tach or V- Fib) isobserved on the monitor and does not produce a pulse. PEA can beany rhythm (sinus, bradycardia, tachycardia). There is organizedelectrical activity without a pulse. Prognosis for PEA invariably is poor unless an underlying causecan be identified and corrected The highest priority of care is to maintain circulation for thepatient with basic and advanced life support techniques whilesearching for a correctable cause

Asystole – AbnormalAsystole refers to the absence of any electrical cardiac activity. It isdefined by 10 non-perfusing complexes per minuteLooking at the ECG you'll see that: Rhythm - Flat or an occasional p wave or QRS complex. TheQRS complexes when they occur are wide and bizarre Rate - 0 Beats per minute QRS Duration - None P Wave - None

ACLS DrugsDrugActionIndicationAdenosineSlows conduction throughthe AV node.Can interrupt reentrypathways in the AV node.Negativechronotropic/dromatropic.Very short half live,Stable narrow complexSVT unresponsive tovagal maneuvers.May consider forunstable narrowcomplex reentrytachycardia whilepreparations are madefor cardioversion.Regular andmonomorphic widecomplex tach thought tobe or previously definedto be reentry SVT.AmiodaroneAntidysrhythmicProlongs duration ofaction potential andeffective refractoryperiod.Increases PR and QTintervals.Decreases sinus rate.Stable VT (preferablyafter expert consult).Recurrent, unstable VT.VF/pulseless VTunresponsive to shockdelivery, CPR ient side effectsinclude flushing, chestpain or tightness, briefperiods of asystole orbradycardia, ventricularectopy.Less effective in patientstaking theophylline orcaffeine.May causebronchospasm, cautionwith asthma patients.Contraindicated inpoison/drug-inducedtachycardia or second orthird degree heart block.Will not terminate atrialfib, atrial flutter or VT.Rapid infusion may leadto hypotension.Do not administer withother drugs that prolongQT interval.*Caution multiplecomplex druginteractionsDosageInitial bolus of 6mggiven rapidly over 1 to 3seconds followedimmediately by a 20mlsaline flushA second dose of 12 mgcan be given in 1 to 2minutes if needed*Reduce initial dose to3mg in patientsreceiving dipyridamole(persantine) orcarbamzepine(Tegretol), in hearttransplant patients or ifgiven by central venousaccess.VT with a pulse: 150mgIV in 50 ml piggybackover 10 minutes.VF/Pulseless VT:300mg IV push, seconddose if needed 150mgIV push.

AtropineAnticholinergic – (parasympathetic blocker)Increase heart rate andAV conduction.Dries secretions.Dilates bronchioles.Decreased GI motility.First line drug for acutesymptomaticbradycardia0.5mg IV every 3 to 5minutes as needed, notto exceed total dose of0.04mg/kg (total 3mg)To control ventricularrate in atrial fibrillationand atrial flutter.Use after adenosine totreat refractory reentrySVT in patients withnarrow QRS complexand adequate bloodpressureUse atropine cautiouslyin the presence of acutecoronary ischemia orMI.Do not rely on Atropinein Mobitz type II secondor third degree AVblock.Should not delayimplementation ofexternal pacing forpatients with poorperfusion.Do not use for wideQRS tachycardias ofuncertain origin or forpoison/drug-inducedtachycardias.Avoid use in patientswith WPW.Blood pressure maydrop.DiltiazemInhibits calcium ioninflux across cellmembrane during cardiacdepolarization; producesrelazation of coronaryvascular smooth muscles,dilates coronary arteries,slows SA/AV nodeconduction times, dilatesperipheral arteriesDopamineCauses increased cardiacoutput: acts on beta 1 andalpha receptors, causingvasoconstriction in bloodvesselsSecond-line drug forsymptomaticbradycardia (afteratropine).Use for hypotensionwith signs andsymptoms of shock.Correct hypovolemiawith volumereplacement first.May causetachyarrhythmias andexcessivevasoconstriction.Usual infusion rate is 2to 20mcg/kg/minTitrate to patientresponse15-20mg (0.25mg/kg)IV over 2 minutes. Maygive another IV dose in15 minutes at 20 to 25mg (0.35mg/kg) over 2minutes

EpinephrineUsed during resuscitationprimarily for is alphaadrenergic effects(vasoconstriction)increasing coronary andcerebral blood flowCardiac arrest: VF,pulseless VT, asystole,PEA.Symptomaticbradycardia afteratropine as analternative to dopamine.Severe hypotensionwhen pacing andatropine fail.Anaphylaxis.Raising BP andincreasing HR maycause myocardialischemia, angina andincreased myocardialoxygen demand.High doses do notimprove survivalCardiac Arrest:1mg (1:10,000) IVadministered every 3 to5 minutes duringresuscitation. Followeach dose with 20 mlNS flushProfound bradycardia orhypotension:2 to 10 mcg per minuteinfusion titrated topatient responseMagnesiumReduces SA nodeimpulse formation.Prolongs conduction timein myocardiumRecommended for usein cardiac arrest only iftorsades de pointes orsuspectedhypomagnesemia ispresent.Life-threateningventricular arrhythmiasdue to digitalis toxicityOccasional fall in bloodpressure with rapidadministration.Use with caution if renalfailure is presentCardiac arrest (due tohypomagnesemia orTorsades de Pointes)1 to 2 g diluted in atleast 10ml of NS orD5W over 5 minutesTrosades de Pointeswith a Pulse of AMIwith hypomagnesemia:Loading dose of 1 to 2Grams mixed in 50 to100 ml NS or D5W over5 to 60 minutes, followwith 0.5 to 1 gram perhour IV (titrate tocontrol Torsades)

Sodium BicarbVasopressinVerapamilAlkalinizing agent –buffers acidosisKnown preexistinghyperkalemia.Known preexistingbicarb responsiveacidosis (DKA,overdose of tricyclicantidepressant, ASA,cocaine ordiphenhydramine).Prolonged resuscitationwith effectiveventilation; on return ofspontaneous circulationafter long arrest intervalNonadrenergic peripheral May be used asvasoconstrictor,alternative pressor to 1stincreasing blood flow toor 2nd dose ofheart and brain.epinephrine inVasopressor effects notVF/pulseless VT,blunted by severe acidosis asystole or PEA cardiacarrest.Adequate ventilationand CPR, not bicarb, arethe major “bufferagents” in cardiac arrest.Not recommended forroutine use in cardiacarrest patients.Potent peripheralvasoconstrictor.Cardiac arrest:One dose of 40 unitsmay replace first orsecond dose of epiSlows depolarization ofslow-channel electricalcellsSlows conduction throughAV nodeDo not use for wideQRS tach of unknownorigin, WPW, sick sinussyndrome or 2nd or 3rddegree heart block5 mg IV over 2 min(over 3 min in olderadults)May repeat 5 mg every15 min as needed tototal dose of 30mgAlternative drug afterAdenosine in SVTTo control ventricularrate in atrial fibrillationand atrial flutter.1 mEq/kg IV bolusOnce ROSC, if rapidlyavailable, use arterialblood gas analysis toguide bicarb therapyDuring cardiac arrest,ABG results are notreliable indicators ofacidosis.

the AHA ACLS course. It includes sections on: ECG Rhythm Interpretation ACLS Drugs ACLS Algorithms . ECG Rhythm Interpretation . Electrical Conduction System SA Node. Primary pacemaker. Rate 60-100 The impulse travels through the raatrial Pathways Int to innervate the atria The impulse reaches the AV Node where electrical activity is delayed to allow for more complete filling of .

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