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EKG Graph Paper

1. e E 30 2nd Degree AV Block Mobitz Type II n 3e nce ER PEENI H ES 2 HS TU at EE E FEE Eu EHE EE HEEL Ein Ieri REL EL H 1 Ex i 1 EEEH PER red DERIT EE EHHI I E 4 LI 1 1 I 1 E T EH EIER i I asm mman ESEA a 222211 E H i tsi ELE zu i EIE as 00 ee 4 rot I Rate Atrial regular Ventricular rate is typically 1 4 to 1 2 the atrial rate depending on the amount of blockage in conduction Rhythm Atrial regular P P is regular Ventricular irregular P waves Upright and normal Some Ps are not followed by a QRS more Ps than QRS PR Interval The PR interval for conducted beats will be constant across the strip QRS Width lt 12 seconds for conducted beats QT lt 40 May be longer with slower heart rates Source of pacer SA Node Characteristics Second degree AV block Type II is also referred to as Mobitz II only two names this time This form of conduction delay occurs below the level of the AV node either at the bundle of His uncommon or the bundle branches common A hallmark of this type of second degree AV block is that there is a pattern of conducted P waves with a constant PR
2. rye ea Hata r pifei Hee T1 m Ep ir c Rate Varies dependine on the underlying rhythm PRI gt 20 sec QRS lt 12 QT lt 40 May be longer with slower heart rates Rhythm Atrial and Ventricle regular Source of pacer SA Node Characteristics First degree AV block is simply a delay in passage of the impulse from atria to ventricles Unlike its name which can be confusing first degree AV block 15 not an actual block but rather a delay in conduction This conduction delay usually occurs at the level of the AV node Remember that in normal sinus rhythm the time it takes the SA node to fire depolarize the atria and transmit to the AV node is lt 0 20 seconds In first degree AV block the patient has a PR interval of gt 20 seconds If the patient s underlying rhythm is sinus bradycardia but the PR interval is 24 seconds the interpretation would be sinus bradycardia with a first degree AV block Causes Acute inferior MI right ventricular infarction increased vagal tone ischemic heart disease digitalis toxicity beta blockers amiodarone calcium channel blockers electrolyte imbalances rheumatic heart disease or myocarditis Nursing Priorities Observe for lengthening PR intervals or development of more serious heart blocks Potential Treatment Treatment for first degree heart block is usually unnecessary as it is typically asymptomatic
3. pr oee EHE E HE E kr 1 m 4 is EHE HE Hi 1 E PA H i S HHE FERAE RHIBGHIEGBLHIGLHHBUE zee 522282 CDPERRBHCOCOWIEC EHEHHHHRHHHUUEHEHHEHEEHEE CE 1 E TIEGBEHHEHEH SEEESESSSSSSESSsS Wh Sas esses cesses SS tH on t r To C r aa E aa HH HERA EET TE EE S EEEEEEEE HA EEA EA HEA L3 EEEEHEHC ECH CHHHHHHEH ss SS g525 22555 S252 52222222222 EE PE EE 2255225555 Rate 40 100bpm Rhythm Irregular QRS Wide If the QRS is wider than 0 16 seconds and with a T wave the opposite direction of the QRS complex the impulse is most generally ventricular PRI P waves absent or retrogra
4. Narrow 30 09 sec Wide 0 09 sec Evaluate QRS duration Probable sinus tachycardia Compatible history consistent with known cause Probable supraventricular tachycardia Compatible history vague nonspecific history of abrupt Possible ventricular tachycardia rate changes P waves absent abnormal HR not variable Infants rate usually 2220 min Children rate usually 2180 min P waves present normal Variable R R constant PR Infants rate usually lt 220 min Children rate usually lt 180 min adenosine if rhythm regular and QRS monomorphic f IO IV access present give adenosine OR f IO IV access not available or if adenosine ineffective synchronized cardioversion 2010 American Heart Association Doses Details Begin with 0 5 1 J kg if not effective increase to 2 J kg Sedate if needed but don t delay cardioversion Adenosine Dose First dose 0 1 mg kg rapid bolus maximum 6 mg Second dose 0 2 mg kg rapid bolus maximum second dose 12 mg Amiodarone IO IV Dose 5 mg kg over 20 60 minutes or Procainamide Dose 15 mg kg over 30 60 minutes Do not routinely administer amiodarone and procainamide together Treatment Determine if child is stable vs unstable If stable attempt vagal maneuver Ice to face If unstable do immediate synchronized cardio version Initial synch dose 0 5 1 joule kg Subsequent synch dos
5. FERTH ELEC Hi E 4 H id b H i L HH 4 i H 1 H m bad I I 1 E N i een LI i i b gt 4 r h f rod IL a x4 die tt E un 4 9 H t fah Hil 1 j a 3 iam a 4 4 masma EIEGON m w lt BEER mcm s m I PT o B j cmm em oam om d occa mm hos 20 Sinus Tachycardia TW Hii imm EL I NU r v rw T Zale Ep EESISHESSISSSESEESEESSESEHSSESHESSHSEESESEESIEEHHE HHIH HH TREE So IT code eee MA IB I LEE j s sb P N 804700 100 150 PRI 12 20 sec lt 12 QT lt 40 Rhythm Regular Source of pacer SA Node Characteristics Sinus tachycardia is a normal response to stress and exercise If it is persistent at rest it may indicate a more severe underlying problem such as fever dehydration blood loss anemia anxiety heart failure hypermetabolic states or ingestion of a significant stimulant such as cocaine or methamphetamine Drugs that can cause Sinus Tachycardia are atropine isuprel epinephrine dopamine dobutrex norepine
6. capture following the pacer spike may or may not occur This can cause lethal arrhythmia Failure to sense can be caused when the sensitivity setting is too low EKG Characteristics Rate It may be regular or irregular Rhythm It can be any intrinsic rhythm in which the pacemaker spike is in the QRS absolute or relative refractory period of the T wave QRS complex It is within the normal limits of the intrinsic rhythm Nursing Priorities amp Potential Treatments Obtain the blood pressure pulse respiratory rate O2 saturation and notify the MD Closely observe for ventricular tachycardia caused by failure to sense Failure to Capture Failure to capture of a pacemaker happens when the output is too low resulting in a failure to depolarize the ventricle which causes an absence of a mechanical contraction of the ventricle or no QRS It can occasionally happen or be constantly happening which results in ventricular standstill and a pulseless patient EKG Characteristics Rate It will be irregular due to the failure to produce QRS Rhythm The pacemaker spike or spikes will not have a QRS following them P Wave It may be absent or present QRS Complex A loss of a QRS behind a pacer spike Nursing Priorities amp Potential Treatments Should the loss to capture be occasional one should get a blood pressure pulse rate respiration rate and O2 saturation This is to determine if the patient is tolerating the failure to capture If the
7. if Heart Rate is gt 100 it 15 called Junctional Tachycardia Rhythm Ventricular rhythm is regular P waves may be absent or may occur before during or after the QRS due to retrograde conduction PR Interval None impulses are originating from the junction not the SA node QRS Width lt 12 seconds the impulse is traveling down the normal pathways of the right and left bundles Characteristics The AV junctional area can speed up and pace at a rate faster than 40 60 beats per minute For all of the same reasons a person might experience a junction escape rhythm a person might also experience enhanced automaticity of the AV junction area The result is a junctional rhythm which depolarizes at a rate of 60 100 bpm This is an Accelerated Junctional Rhythm If the rate is greater than 100 bpm the rhythm is called Junctional Tachycardia see above It might be tempting to call the ECG tracing a normal sinus rhythm but make note that uniform looking P waves are absent along with a constant PR interval The SA node is not working and the junction has taken over as the pacer only a bit faster than its normal intrinsic rate of 40 60 bpm Possible Causes of Accelerated Junctional Rhythm Digoxin toxicity most common cause Hypoxia cardiomyopathy MI and or Valve replacement surgery Nursing Priorities Check your patient s blood pressure assess for syncope palpitations or SOB Lower blood pressure may result from loss of atrial ki
8. 40 sec with slower ventricular rhythms P waves Upright and normal Rhythm Rhythm P P is regular R R is regular but the two are independent functions Source of pacer Variable Will be below the atria since the connection between the SA Node and AV Node has been severed Usually Junctional or Ventricular in origin Characteristics Third degree AV block is also called complete heart block This type of dysrhythmia indicates complete absence of conduction between atria and ventricles the atria and the ventricles are not communicating with one another The atrial rate 15 always equal to or faster than the ventricular rate in complete heart block The block may occur at the level of the AV node the bundle of His or in the bundle branches As in second degree AV block this distinction is not merely academic since pathogenesis treatment and prognosis may vary considerably depending on the anatomic level of block When third degree AV block occurs at the AV node a junctional escape pacemaker frequently will initiate ventricular depolarization This is usually a stable pacemaker with a rate of 40 to 60 beats per minute Since it is located above the bifurcation of the bundle of His the sequence of ventricular depolarization usually is normal resulting in a normal QRS This type of third degree AV block can result from increased parasympathetic tone associated with inferior infarction from toxic drug effects e g digitalis propranolol or
9. Characteristics Ventricular Tachycardia VT is defined as three or more consecutive PVCs in a row at a rate greater than 100 beats per minute VT is generally caused by single foci in either ventricle that fire at a rapid rate to override the SA node and thereby take control of the heart s rhythm A short run of consecutive PVCs is often called a burst of VT ECG characteristics include rapid regular rhythm with a wide QRS The QRS is wide since the origin of the rhythm is outside the bundle branches thereby taking a longer time to conduct cell to cell within the ventricle Ventricular tachycardia may be monomorphic all QRSs with the same shape or polymorphic varying QRS shapes during the tachycardia This arrhythmia may be either well tolerated or associated with life threatening hemodynamic compromise The hemodynamic consequences of VT depend largely on the presence or absence of myocardial dysfunction such as might result from ischemia or infarction and on the rate of VT the faster the rate the less well tolerated Causes Ventricular tachycardia may be caused by R on T PVC phenomenon hypoxia ischemia AMI acidosis cardiomyopathy mitral valve prolapse digitalis toxicity antiarrhythmics electrolyte imbalances liquid protein diets increased intracranial pressure and central nervous system disorders Nursing Priorities Check your patient s pulse and blood pressure to determine if this is stable unstable B P lt 90 o
10. H 1 i a L 1 i a i i 1 1 a s I 1 i 1 i 1 a i li i 4 Et TE Li i _ o 8 i T 1 t i amp Mo r k c Li L 17 1 1 r re n gt L 1 1 1 I j 1 1 1 i i L L I i pres I i 2 f I H H 1 k i E i 1 a ji Adsl j 1 i 1 E es i 1 ERIS A EET W zx 1 ha lt a xq k 1 4 1 i I T jx 1 1 1 n a i a 4 I 1 1 1 1 E x 1 1 1 3 B Me ee M rr a 1 1 i 1 1 i 39 Polymorphic Ventricular Tachycardia Torsade de Pointes Y zd 12 22 k 12 22 SaaS LEAD II A Hi AI EIE eve UP E V V We JU Ap U V V tene MA ij Veiis F w i EE ieee EE s Rate 100 250 BPM PRI P waves may be present if SA node is functional however there is no relation to the QRS It is unlikely that P waves will be visible since this rhythm typically moves at a very fast rate and the P waves will be buried in the QRS QRS Wide Bizarre gt 12 QT Usually lt 40 seconds due to fast heart rate Rhythm Usually regular Source of pacer Ventricular Purkinje
11. Interval QTD The QTI represents the refractory period of the ventricles The QT interval represents total ventricular activity as they depolarize and repolarize It begins with the first wave in the QRS complex representing ventricular depolarization and ends when the T Wave returns to baseline at the isoelectric line representing ventricular repolarization As rule of thumb a normal QTI is less than 0 40 seconds The QTI is directly related to the heart rate _ BER ERE ERR _ _ LI eoll ERE Sie _ ERE Ain 114 998 Normal Measurements of 0 36 0 40 It is best to measure the QTI in a lead in which the T wave is most pronounced The normal overall length of the QTI should be equal to or less than 1 2 of interval Summary of Heart Measurements P Wave Upright in lead II PRI 0 20 Sec QRS 0 12 Sec ST Segment Even with isoelectric line T Wave Upright in lead II QTI 0 40 Sec SERRE LL LL LLLI ERE LI 441 See AAAI lI MRI PLII II EELEZNEN EN L L LEEEEP TTS EI aol ti L I 1 1 zz mars mm Rate Measurement The patient s heart rate reveals a great deal of information If the rate is slow under 60 beats per minute we call it bradycardia If the heart rate is fast over 100 beats per minute then it is called tachycardia EC
12. and T wave in a direction opposite to the QRS complex After the PVC occurs you may find a short pause before the next QRS This is called a compensatory pause The compensatory pause may or may not be present Unifocal PVCs When a PVC originates from a single focus its morphology or waveform characteristics look the same each time When a PVC looks the same each time it 15 called a unifocal PVC ecause it originates from one area All of the PVCs from a unifocal source are identical in appearance The strip below is an example of a unifocal PVC Multifocal PVCs In cases of greater irritability several ventricular foci might begin to initiate ectopic beats Multifocal PVCs will occur if more than one ectopic area begins to initiate early ventricular beats For example if three ectopic ventricular sites began initiating PVCs each site would produce a slightly different looking PVC waveform The ECG criteria are basically the same as unifocal PVCs Multifocal PVCs are considered more dangerous when compared to unifocal PVCs as this represents a greater amount of myocardial irritability Below is a sample of a patient in NSR with a couplet of PVCs from two foci multifocal PVCs may also occur in succession When this happens the PVCs are called a Couplet The strip above also shows a couplet The term Ventricular Bigeminy is used for a grouped beating pattern when every other beat is a PVC despite the underlying rhythm For example ve
13. bizarre Ventricular None None None None No electrical activity Asystole 18 Types of Rhythm Normal Sinus Rhythm 1 TEES FAAS it i i l L 1 k 4 T ae ii 1 8 gt 1 LI li 1 s 1 T I i L LLEI 1 LI LL 1 i em om aks I T I I T 4 I 44 1 ama 3 1 1 1 i i 1 P N Boul To Rate 60 100 BMP PRI 12 20 sec QRS lt 12 QT lt 40 Rhythm Regular Source of pacer SA Node Characteristics Normal sinus rhythm NSR is the characteristic rhythm of the healthy human heart NSR is considered to be present if the heart rate 15 in the normal range the P waves are normal on the ECG and the rate does not vary significantly If however the R R interval is variable the rhythm is called sinus arrhythmia The normal heart rate has been considered to be between 60 and 100 beats min However the range defined by two standard deviations from the mean is between 43 and 93 beats min in men and 52 and 94 beats min for women there is also important variability in age in young children The normal heart rate is 110 to 150 beats min in infants with gradual
14. from damage to the AV node When third degree AV block occurs below the junction it is most often due to a block involving both bundle branches The only escape mechanism available is in the ventricle distal to the site of block Such a ventricular escape pacemaker has an intrinsic rate that is slow less than 20 40 beats per minute Like any depolarization originating in a ventricle the QRS complex will be wide It is not a stable pacemaker and episodes of ventricular asystole are common Remember that the rhythm strip reflects two separate processes that are taking place The SA node continues to control the atria and typically fires at a rate of 60 80 bpm Since the atria and the ventricles are not communicating one of the two remaining back up intrinsic pacemakers will take over Either the junction will pace the ventricles rate 40 60 bpm or the back up ventricular pacer will discharge rate 20 40 bpm When there are two separate pacemakers controlling the upper and lower chambers of the heart without regard to each other the situation is called AV disassociation this is not a rhythm but a condition and the umbrella term AV disassociation 15 often used On the ECG you will see normal P waves marching regularly across the strip The P P intervals are regular You will also see QRS complexes at regular intervals The unique feature is that the P waves and the QRS complexes will not be talking to each other There is no relat
15. in VF the more difficult it is to convert the rhythm Potential Treatments Initial treatment is always defibrillation Only defibrillation provides definitive therapy Other priorities include securing an airway making sure the patient has IV access and administering medications per guidelines 38 Asystole J F Je c4 ELLA k 12 24 3MRYB3 LEAD ls a cH E See i H as Ese E n ee eee m r of oc EE m aram bonnm eS i i wa E mmm H 14 ated S25 Sees Fasc Rate None P waves None Nursing Tip Assess your PRI None patient Treat the patient QRS None and not QT None the monitor Rhythm None Source of pacer None Characteristics Asystole represents the total absence of electrical activity Since depolarization does not occur there is no ventricular contraction and a straight line will appear on the ECG To assure there is no electrical activity check the rhythm in a second lead and make sure your monitor is working properly Asystole may occur as a primary event in cardiac arrest or it may follow VF In addition the distinction between very fine VF and asystole may be very difficult If it might be VF it should be treated like VF with defibrillation If no organized QRS complex is seen and the patient has a pulse then the ECG is improperly connected turned off or improperly
16. on the lead wire one placed on the R atrium amp one on the R ventricle Artificial impulses stimulate or pace first the atria then the ventricles H Le HUS lai Automat interval Rules for interpretation of Pacemaker Rhythms Same as for dysrhythmias Remember Properly functioning pacemakers will produce rhythms with pacemaker spikes Spikes indicates only that the pacemaker is firing They do not reveal information relative to ventricular contraction Assess your patient for presence of symptoms Identify patient s own rhythm and rate Identify the pacemaker rate Measured pacer spike to pacer spike What type of complex does the spike produce P waves QRS waves Does every pacemaker spike produce a complex capture Is the pacer sensing the patient s rhythm correctly Code System 1 letter chamber being paced 2 letter chamber sensed A atrium A atrium V ventricle V ventricle D dual both D dual both O off 3 letter type of response by pacemaker to sensory 4 letter ability of generator to be programmed I Inhibited pacemaker will not function when the O none person s heart beats P Simple programmability O none M Multi programmability T triggered C Telemetry ability D dual P ability of rate to change with activity 5 letter ability of generator to defibrillate P Antitachycardia S Shock D antitachycardia processing amp shock O none Common Problems associated with Pacemakers Battery failure Decreased amp
17. slowing over the first six years of life The P waves are upright and precede the QRS complexes The PR interval is less than 20 seconds and the QRS complex is 06 12 sec Nursing Priorities None Potential Treatment None 19 Sinus Bradycardia Rate lt 60 BPM PRI 12 20 sec QRS lt 12 QT lt 40 May be prolonged with excessively low heart rates Rhythm Regular Source of pacer SA Node Characteristics This rhythm may be normal for well conditioned athletes and during sleep Sinus Bradycardia may be caused by several factors such as increased vagal tone from vomiting bearing down to have a bowel movement or from medications such as digitalis calctum channel blockers beta blockers and many other antiarrhythmic medications Common with inferior wall MI obstructive jaundice and increased intracranial pressure ICP Nursing Priorities Check your patient s blood pressure assess for syncope and SOB Patient may need to lie down to prevent potential falls Keep in mind that it may be normal for some individuals to have sinus bradycardia e g athletes Potential Treatment Treatment is only necessary if the patient is symptomatic Atropine 0 5 1 0 mg to a maximum of 3mg Consider external transcutaneous pacing Be prepared to assist the physician with the placement of an external temporary pacer Treatment of associated hypotension may also need to be addressed la a PA Mer LN
18. so the pacemaker appropriately inhibited and reset it s automatic interval at the peak of the QRS EKG Characteristics Pacer misinterprets other electrical activity as a QRS Pacer fires at a rate slower than the preset rate Pacer does not fire when expected Pacemaker spikes appear further away from intrinsic or paced complexes than expected based on the automatic interval Nursing Priorities amp Potential Treatments Bradycardia hypotension Dizziness syncope diaphoresis amp Chest pain Since the pacemaker is firing less than expected the patient will have a return of symptoms that lead to pacemaker insertion Remember in under sensing we said you would see over pacing In over sensing you will see under pacing You will expect the pacemaker to produce a pacer spike and it does not Atrial Pacing In front of P wave One pacer spike per P wave Ventricular Pacing In front of QRS One pacer spike per QRS Pacemaker Summary AV Pacing In front of both P wave amp QRS One or Two pacer spikes per PORST complex Loss of Capture Pacer spike not followed by a complex 46 Failure to Pace No pacer spikes Over Sensing Pacer spikes not occurring as expected too far away from intrinsic complexes Under Sensing Pacer spikes too close to intrinsic complex Conclusion This review guide has taught the anatomy physiology and basic electrophysiologic knowledge needed to understa
19. the ventricular myocardium It can be regarded as a backup plan or redundancy built into the body Causes Myocardial Infarction Pacemaker Failure Metabolic imbalance Myoardial Ischemia Nursing Priorities Asses patient measures to improve cardiac output and establish a normal rhythm and rate Potential Treatments Atropine 0 25 1 mg is sometimes used to accelerate underlying sinus rate to inhibit IVR Isopreterenol verapamil and antiarrhythmia drugs such as lidocaine and amiodarone are occasionally used for IVR Pacing Caution Suppressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill IN 41 Accelerated Idioventricular AIVR poe pL pe HITETETEREEEEFEEEEHEHEEE 355522222 222225222 FEE FIT FERTA GGG cee SESSE EE SSES u FEH HES 5522225222 25222 2222222 SS 55555 ER E E FEEEHEREEHEEEEEEHEHH EE EH EG iub iii E EE AEE X Re eee AES FI web KIWI
20. 0 000 concentration Repeat every 3 5 minutes If no IO IV access may give endotracheal dose 0 1 mg kg 0 1 mL kg of 1 1000 concentration Amiodarone IO IV Dose 5 mg kg bolus during cardiac arrest May repeat up to 2 times for refractory VF pulseless VT Advanced Airway Endotracheal intubation or supraglottic advanced airway Waveform capnography or capnometry to confirm and monitor ET tube placement Once advanced airway in place give 1 breath every 6 8 seconds 8 10 breaths per minute Return of Spontaneous Circulation ROSC Pulse and blood pressure Spontaneous arterial pressure waves with intra arterial monitoring Reversible Causes Hypovolemia Hypoxia Hydrogen ion acidosis Hypoglycemia Hypo hyperkalemia Hypothermia Tension pneumothorax Tamponade cardiac Toxins Thrombosis pulmonary Thrombosis coronary Basic Characteristics of Cardiac Rhythms P R QRS Sinus 60 100 Regular 0 12 0 20 sec 0 12 sec Rhythms Normal Sinus Sinus lt 60 Regular 0 12 0 20 lt 0 12 sec Bradycardia Sinus 100 160 Regular 0 12 0 20 sec lt 0 12 sec Tachycardia Sinus 60 100 Irregular 0 12 0 20 sec lt 0 12 sec Rhythm varies with Arrhythmia respiration Sinus Depends on Usually regular 0 12 0 20 sec 0 12 sec Pause Arrest pauses with pauses Depends on Interrupts 0 12 0 20 sec 0 12 sec Regularity depends underlying underlying on underlying rhythm rhythm an
21. Banner Staff Service ECG Study Guide Edited by Larry H Lybbert MS RN Banner Staffing Services Table of Contents a uuu ean ECG INTERPRETATION BASICS uu 4 AI A IDLIL AIERNL L u E 9 TS STS CO VI O aAA 9 TS EE k i OG unun au amana m 9 l O 9 IS GUIDE 11 13 Six Basic Steps for Rhythm Interpretation Summary 13 NURSING PRIORITIES AND POTENTIAL TREATMENTS scssovstscidscces dosevoascunscesimasaceisdinossiacaneaecoumnccaiaspueasciesaotaeiaeconiens 14 TAY G 14 PEIEE ERROR To Qo Ve 16 BASIC CHARACTERISTICS OF CAR DIAC tele 17 TYPES PR THV eei ET 19 ENS uu 19 ADITI V uuu u 20 SINUS EAC IP Roses 21 PREV ATURE ATRIAL CONTRACTIONS PACS h uuu u a aasan NODE REFUGE 23 PEN SI SUBE TI NT 24 S
22. Fibers Characteristics Polymorphic ventricular tachycardia PVT is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude axis and duration The commonest cause of PVT is myocardial ischaemia Torsades de pointes TdP is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation it has a characteristic morphology in which the QRS complexes twist around the isoelectric line For TdP to be diagnosed the patient has to have evidence of both PVT and QT prolongation Torsade de Points is essentially a polymorphic VT It is characterized by a widening and narrowing of the QRS amplitude The arrhythmia may be paroxysmal which starts and stops suddenly and may suddenly deteriorate into VF Bidirectional VT is another type of polymorphic VT most commonly associated with digoxin toxicity Causes The cause of Torsades may be reversible The most common causes are drugs that lengthen the QT interval such as antiarrhythmics quinidine procainamide and stalol Other causes include myocardial ischemia and hypokalemia hypomagnesemia and hypocalcemia Nursing Priorities Unstable patients have signs or symptoms of insufficient oxygen delivery to vital organs as a result of the tachycardia Such manifestations may include the following Chest pain Dyspnea Hypotension Altered level of consciousness Potential Treatments Find and trea
23. G monitors display the heart rate When an ECG strip is printed most printers provide heart rate information at the top of the strip Never the less you might be in a situation where you must calculate the heart rate from the ECG recording There are numerous methods and formulas which can be used to calculate a heart rate from the ECG Three methods for heart rate calculation are presented below The Six Second Method This method can be used with either regular or irregular rhythms and provides a rough estimate but not precise of heart rate Print a 6 second strip see text box 1f you are not sure how to do this Count the number of R waves in a 6 second strip and multiply by 10 For example if there are seven 7 R waves in a 6 second strip the heart rate 1s R R R R R R approximately 70 or 7x10 70 Let s give it a try Look at the rhythm below and count all the R waves Large Box Method Count the number of large squares between two consecutive R waves Divide this number into 300 for a ventricular rate For example if there are four large squares between regular QRS complexes the heart rate 15 75 300 4 75 For an atrial rate count the number of large boxes between two consecutive P waves and also divide into 300 Small Box Method This method also uses an R to R or P to P measurement but is more precise because we use the smaller ECG boxes to help us calculate the heart rate To calculate the ventr
24. IE DERE u s 25 PBI S BENE o 26 ACCELERATED JUNCTIONAL RHYTHM JUNCTIONAL TACHYCARDIA ecce eene nene nnn eenn nnne ener n nennen 21 AURIOVENIRICUEAR DEOGRS 28 IST GRE Ay NI I Kuu sun Lun u N ua Zuna 29 2ND DEGREE AV BLOCK MOBITZ TYPE L WENCKEBACH a sense eese serena 29 2ND DEGREE FeV BOCK NIOpIiIZ T SPESE uuu 31 SRD DEGREE AB BLOCK COMPLETE HEART BLOCK 32 34 PREMATURE VENTRICULAR CONTRACTION 35 VENTRICULAR TACHYCARDIA u u 257 VENTRICULAR T I I Pi j K x 38 A TOT 39 POLYMORPHIC VENTRICULAR TACHYCARDIA TORSADE DE POINTES_ 40 IDIOVBNTEICUEASR eaa a EE A E E E A 41 ACCHERATFDIDIOVENTRICULAR AIVR ETE E ES 42 PACTOTA uu TO Tm 43 Pacemgk OF u u uuu 2 uuu 46 CONCLUSTON 5 47 ECG Study Guide ECG Assessment Testing 1s an assessment of your basic knowledge and should be completed as part of your new hire process Although we are sure that you know the information you need to study this information to be prepared to pass the test Please remember the following guidelines The study guide is a good overall review of the components of the ECG waveform and more common dysrhyth
25. Treatment typically aims to correct the underlying cause Consult with physician if PR interval is lengthening Discuss holding medications which slow A V conduction 29 2nd Degree AV Block Mobitz Type I Wenckebach Rate Atrial regular Ventricular rate is slightly slower Typically between 60 90 bpm Rhythm Atrial regular Ventricular irregular due to dropped P waves P waves Upright and normal Some P s are not followed by a QRS more Ps than QRSs PR Interval Progressively longer until one P wave is not followed by a QRS complex After the blocked beat the cycle starts again QRS Width lt 12 seconds QT lt 40 May be longer with slower heart rates Characteristics Second degree AV block Type I is unique in that it has three different names and all three are used interchangeably just to keep us all on our toes Second degree AV Block Type I is also called Mobitz I or it can be referred to as Wenckebach Do not let this confuse you as all three names mean the SAME rhythm For simplicity we will call this rhythm Wenckebach Wenckebach is characterized by a progressive prolongation of the PR interval so the key to diagnosing this rhythm is by careful examination of each PR interval The SA node is healthy and fires on time thus the P to P intervals are regular Impulses traveling through the AV node take longer and longer to fully conduct until one impulse is completely blocked The SA node continues to fire rig
26. a T s Tension pneumothorax Tamponade Toxins Thrombosis Thrombosis Pediatric Cardiac Arrest Shout for Help Activate Emergency Response CPR 2 min O IV access Rhythm No shockable Yes 5 Shock CPR 2 min Epinephrine every 3 5 min Consider advanced airway Rhythm shockable Yes 7 f Shock CPR 2 min Amiodarone Treat reversible causes Start CPR Give oxygen Attach monitor defibrillator 10 9 Asystole PEA O IV access Epinephrine every 3 5 min Consider advanced airway Asystole PEA 10 or 11 CPR 2 min Rhythm Yes No CPR 2 min Treat reversible causes Rhythm Yes shockable e Organized rhythm check pulse Pulse present ROSC post cardiac arrest care 16 2010 American Heart Association Doses Details CPR Quality Push hard 21 3 of anterior posterior diameter of chest and fast at least 100 min and allow complete chest recoil Minimize interruptions in compressions Avoid excessive ventilation Rotate compressor every 2 minutes If no advanced airway 15 2 compression ventilation ratio If advanced airway 8 10 breaths per minute with continuous chest compressions Shock Energy for Defibrillation First shock 2 J kg second shock 4 J kg subsequent shocks 24 J kg maximum 10 J kg or adult dose Drug Therapy Epinephrine IO IV Dose 0 01 mg kg 0 1 mL kg of 1 1
27. an If symptomatic bradycardia is present administer atropine and apply transcutaneous pacemaker Atropine may be effective if the QRS is narrow AV node level of block but has little or no effect on wide QRS bundle branch level third degree block rhythms Administer a dopamine infusion if patient 15 hypotensive x Ac m REEMA reeset Hue 33 Ventricular Rhythms All of the dysrhythmias which you have learned thus far are classified as supraventricular dysrhythmias because they originate from above the ventricles When a rhythm originates from above the ventricles and thereby travels down the normal right and left bundles to the Purkinje fibers the QRS is 12 seconds or less When rhythms originate in the ventricles they generally have a QRS gt 12 seconds because they are coming from an area outside the right and left bundle branches This is an important concept to remember Ventricular rhythms are of great importance and can be very dangerous Our hearts were designed to conduct and contract from the top down atria to ventricle When this mechanism is disrupted we lose our atrial kick and the heart s efficiency is greatly reduced The first dysrhythmia is not an actual rhythm but an occasional ectopic abnormal beat originating from an irritable cluster of cells somewhere in either the right of left ventricle Left atrium AV node Left ventricle Right Bundle
28. and Holtz 18 PR interval the primary clue to the degree of heart block QRS width Dropped QRS complexes pauses Second degree Mobitz 1 Wenckebach Atrial rate generally at intrinsic rate of 60 min to 100 min Ventricular rate depends on number of impulses conducted through atrioventricular node will be slower than atrial rate ERR irregular P to P wave is constant 1 1 until block occurs then a P wave with a pause absent of a QRS complex then cycle restarts with a P wave and associated QRS complex Variable PR interval progressively lengthens until a QRS complex is dropped A pause follows the dropped QRS complex then PR interval resets to shorter interval and the cycle repeats very cyclic Normal 0 12 s Yes pattern of progressive lengthening of the interval from QRS to QRS until a QRS is dropped after a P wave then a pause occurs and theinterval resets Second degree Mobitz type 2 Complete or third degree Atrial rate generally at intrinsic rate of 60 min to 100 min Ventricular rate depends on number of impulses conducted through atrioventricular node may intermittently be the same as atrial rate when impulses are being conducted Ventricular rate will be slower than atrial rate when impulses are blocked Regular Regularly irregular or irregularly irregular P to P wave is constant 1 1 until block occurs then 2 or more P waves that are follo
29. ative deflection following the R Wave below the isoelectric line Prime is a secondary positive wave that may represent abnormal ventricular conduction Below are examples of the shapes that the QRS complex may take R R R Q S Q QS S ST Segment Represents early ventricular repolarization and extends from the end of the QRS to the beginning of the T Wave it is normally even with the isoelectric line A deviation either above or below the isoelectric line represents myocardial injury or ischemia Basic facts of the ST segment The ST segment starts at the end of the QRS and ends at the start of the T Wave The ST segment represents the early beginning of ventricular repolarization The portion of the EKG tracing where the QRS ends and the ST 5mm segment begins 15 called the J Point Lo 5mm SE CO at CM sidadas LLLI ne ea Te CU ag 0 5 mv OT Interval Characteristics The ST segment normally remains Isoelectric which is the normal baseline of EKG Elevation greater than Imm in two or more reciprocal leads may indicate injury Depression greater than Imm in two or more reciprocal leads may indicate myocardial ischemia T Wave Represents ventricular repolarization as the ventricles return to a state of relaxation The T Wave 15 typically rounded and systematical The T Wave 15 typically upright however this may vary if myocardial injury or ischemia is present QT
30. calibrated Causes End stage cardiac disease ischemia MI severe electrolyte imbalances acidosis and hypoxia Nursing Priorities Check rhythm in a second lead make sure a lead has not fallen off If your patient has a pulse they are obviously NOT in asystole If the patient is pulseless initiate CPR and call for help Potential Treatments Continue CPR and secure airway and IV access Search for possible causes Implement medication therapy per ACLS guidelines ar t 1 i 4 t Se ss lt lt i i i i n L i F w oe k td 2 i i a H 1 i I a Y 1 fs ee 1 1 i 1 I w i i i i i frizat a f k i i L E be 1 T f a n Ld f b I f ie eee as s s i k i d L 4 4 F i r i i t i 1 1 a 4 gt m 8 h 4 1 i 1 1 1 H i L T i Wa za Ww 4 1 lt lt i F I I i a a 1 i 1 1 i i t b 1
31. cally centered around observation and monitoring for increased frequency Be aware that individuals may complain of palpitations or feeling a skipped heart beat with an irregular pulse Explain to them the reason for these feelings Increased number of PACs may be a forerunner of the development of atrial fibrillation or other atrial dysrhythmias 20 Atrial Fibrillation PRI None QRS lt 12 sec QT lt 40 Rhythm Irregular Source of pacer Atrial Characteristics Atrial fibrillation is caused by chaotic ectopic or reentry current activity which causes the atria to quiver rather than contract The atria quiver at a high rate producing the fuzzy and garbled wave forms seen where a flat isoelectric line should be Atrial fibrillation can generate a ventricular response rate that is controlled or very fast and can place the patient at risk for hemodynamic instability Cardiac output is reduced with the loss of Atrial Kick since the atria are not contracting The ventricular rate my also be very fast resulting in further decreased cardiac output In addition since the atria are not contracting the patient is at risk for the formation of emboli leading to pulmonary embolism or stroke Causes MI Rheumatic heart disease COPD CHF ischemia chest trauma CAD and open heart surgery Treatment Treatment may very If this is an acute arrhythmia the patient may be cardioverted or treated with beta blockers calcium chann
32. ck Potential Treatments Asymptomatic Observation Symptomatic Discontinue digoxin therapy Check potassium levels If heart rate becomes faster 100 180 bpm the rhythm 15 called Junctional Tachycardia Now consider treatment with IV amiodarone beta adrenergic blockers Esmolol Labetalol Metoproplol or calcium channel blockers Junctional Tachycardia 27 Atrioventricular Blocks Atrioventricular blocks otherwise known as heart blocks can be divided into three degrees First degree heart blocks are characterized by P to R intervals longer than 0 20 seconds Second degree heart blocks are characterized by some P waves being blocked at the AV node This results in some P waves occurring without following QRS complexes Third degree heart block 15 characterized a complete dissociation between P waves and QRS complexes Nursing Tip A hint for separating the heart blocks into degrees is that first and third degree blocks usually have regular QRS rates Differences Between First Degree Second Degree And Complete Heart Block of heart block Prec WoC analoer apie appearance Rate Generally at intrinsic rate of 60 min to 100 min May be slower Regularity of atrial Regular rhythm ventricular rhythm P to P wave is constant P QRS ratio Constant PR interval but prolonged gt 0 20 s or 200 ms Normal lt 0 12 s a Adapted from Huff17 and Garcia
33. d number of PAC s i 150 250 Regular 0 12 0 20 sec 0 12 sec P waves may be Tachycardia hidden in previous T SVT due to rapid rate Atrial Flutter V rate varies Irregular Variable 0 12 sec Sawtooth pattern F A rate 250 waves 350 Atrial Controlled gt 100 Irregular Nonmeasureable Fibrillation 100 0 12 sec Uncontrolled AF Wandering 60 100 Irregular 0 20 sec lt 0 12 Morphology of P Pacemaker wave changes Heart Blocks 60 100 Usually regular gt 0 20 sec 0 12 sec P QRS ratio 1 1 Ist AV block 2nd Degree V lt A Atrial regular Progressively 0 12 sec P QRS ratio 1 1 Mobitz 1 Ventricular longer until one Wenkebach irregular QRS dropped 2nd Degree Remains Atrial regular variable Mobitz II Constant Vent regular or irregular 40 60 Junct p p regular Nonmeasurable MEM More P s than QRS s More P s than QRS s 20 40 Vent r r regular P R QRS Junctional 40 60 Regular 0 12 sec if 0 12 sec Escape present Accelerated 60 100 Regular 0 12 sec if 0 12 sec Junctional present i 100 180 Reeular lt 0 12 sec 1f lt 0 12 sec Tachycardia present Interrupts No PR interval gt 0 12 sec wide underlying rhythm and bizarre Ventricular 150 250 Regular No PR interval gt 0 12 sec wide Tachycardia and bizarre Ventricular No cardiac Irregular No PR interval No QRS Chaotic Fibrillation output Idioventricular 20 40 Regular No PR interval gt 0 12 sec Slows as heart dies
34. de conduction Characteristics Accelerated idioventricular rhythm AIVR is a relatively benign form of ventricular tachycardia It often occurs during reperfusion after a myocardial infarction It has a frequency of 60 120 bpm mostly 80 100 AIVR used to be a good sign as it made clear that reperfusion was succeeded especially after thrombolysis where the success cannot easily be determined without angiography However recently debate has started whether among patients with successful coronary intervention AIVR 15 a sign of ventricular dysfunction and therefore a slightly worse prognosis Causes Myocardial Infarction Pacemaker Failure Metabolic imbalance Myoardial Ischemia Nursing Priorities Asses patient measures to improve cardiac output and establish a normal rhythm and rate Potential Treatments Atropine 0 25 1 mg is sometimes used to accelerate underlying sinus rate to inhibit IVR Isopreterenol verapamil and antiarrhythmia drugs such as lidocaine and amiodarone are occasionally used for IVR Pacing Caution Suppressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill 42 Paced Rhythms Rate Determined by Pacemaker PRI lt 20 QRS Variable based on type of pacer Rhythm Regular Source of pacer Pacemaker Characteristics Device that substitutes for the normal pacemaker of the heart s electrical conduction s
35. e ventricles When the ventricular rate is 100 bpm we call this controlled atrial flutter If the ventricular rate is gt 100 bpm it is labeled uncontrolled atrial flutter Since ventricles always have more time to fill during diastole when the HR is under 100 our goal 1s to have controlled atrial flutter This can often be accomplished with drug therapy In the setting of atrial flutter coordinated contraction of the atria is absent The patient has therefore lost their atrial kick with potential loss of cardiac output and lower blood pressure Causes Acute or chronic cardiac disorder mitral or tricuspid valve disorder cor pulmonale pericarditis Post MI complication usually transient Hyperthyroidism Alcoholism Post cardiac surgery usually transient Nursing Priorities Check your patient s blood pressure assess for syncope palpitations or SOB Your patient may need to lie down to prevent potential falls Patient may have lower B P due to loss of atrial kick Potential Treatments Asymptomatic Observation and rate control Normal heart function control ventricular rate by administering beta blockers esmolol or calcium channel blockers diltiazem or verapamil Impaired heart function control ventricular rate by administering digoxin diltiazem or amiodarone Symptomatic If hemodynamically unstable synchronized cardioversion at 100 200 monophasic joules mu m MEN
36. el blockers digoxin amiodarone or procainamide If this is a chronic rhythm that would not convert with cardioversion or medications it is important that the patient be evaluated and possibly placed on anticoagulation medication before discharge home chee HP SPE E NE E 24 Atrial Flutter pee Rate Atrial rate is 250 350 bpm Ventricular rate varies according to AV node conduction Rhythm Atrial regular ventricular may be regular or irregular again depending on AV node conduction P waves Absent Only flutter or saw tooth looking waveforms PR Interval Not applicable QRS Width lt 12 seconds Characteristics Atrial Flutter is a dysrhythmia which is the result of a flawed reentry circuit within the atria It 15 often described as resembling a sawtooth or picket fence These flutter waves should not be confused for P waves The AV node is a wonderful protective mechanism Imagine the atria depolarizing at a rate of 250 to 350 bpm If all of these atrial depolarizations were conducted down into the ventricle the patient s ventricles would likely begin to fibrillate Think of the AV node as the central train station where numerous train tracks merge The central station only lets some of the trains through to avoid congestion The AV node helps to protect the ventricles by only allowing some of the atrial depolarizations to conduct down through the bundle of His into the bundle branches and on to th
37. ervices 480 684 6428 480 684 6427 Larry Lybbert bannerhealth com Angela Stone bannerhealth com ECG Interpretation Basics EKG Graph Paper The paper used to record EKG tracings is grid like in nature and has specific markings utilized to mark length in seconds The paper is divided into large and small boxes Thicker darker lines separate large boxes thinner lighter lines separate small boxes e The dark vertical lines are 0 20 seconds apart The lighter vertical lines are 0 04 seconds apart Each small box is 1mm in size Each small box represents an electrical current that is equal to 0 1 millivolt mV One mV 15 equal to two large boxes 0 20 Sec EIE 0 5 mV 1mm 0 04 Sec Pe ye DENEN Seconds TE Normally EKG graph paper has thick dark lines at the top or bottom of the paper In the strip presented here the lines are at the bottom of the paper The space between the lines is equal to 3 seconds A standard EKG strip is run over 6 seconds When printing an EKG rhythm strip the paper prints at a standard speed of 25 mm per second omponents of the Normal EKG Waveform FONS ae ce esa k m E LLLLLLLRA TERRE 101015201111 ptt ttt tt IJ p kl The EKG 1s a real time recording of the hearts electrical activity produced by depolarization repolariza
38. es 2 joules kg Consult cardiology Get a 12 lead EKG but do not delay treatment to obtain EKG For SVT resistant to vagal maneuvers Adenosine 0 1 mg kg max Ist dose 6mg Rapid 2 syringe technique VT with pulses Wide QRS Uncommon in children HR Normal for age to 2200 Treat underlying causes possibly due to hyperkalemia hypocalcemia hypomagnesaemia toxins Treatment for stable VT w monomorphic ORS Adenosine 0 mg kg IV IO Ist dose 6 mg max Adenosine 0 2mg kg IV IO 2nd dose 12mg max Expert consultation Amiodarone 5mg kg over 20 60 minutes OR Procainamide 15mg kg over 30 60 minutes Unstable VT Synchronized cardioversion 0 5 to J kg may increase to 2j kg if ineffective For VT refer to algorithms 15 Cardiac Arrest Shockable rhythm Pulseless VT or VF Start CPR at least 100 compressions min with good chest recoil change compressors Q2 mins Assess cardiac rhythm Shock immediately if VT or VF 2 j kg Ist dose 4j kg subsequent doses repeat every 2 minutes Epi 0 1ml kg every 3 5 minutes Amiodarone 5mg kg DEAD Defib Epi Amiodarone Defib Non shockable rhythm Asystole PEA NO defib NO Amio for Asystole or PEA Start CPR at least 100 compressions min with good chest recoil change compressors Q2 mines Assess cardiac rhythm Epi 0 1 ml every 3 5 minutes Identify amp treat reversible causes H s Hypovolemia Hypoxia Hydrogen ion acidosis Hyper hypokalemia Hypoglycemia Hypothermi
39. failure to capture is continuous the patient will be pulseless or have a symptomatic bradycardia This can range from a situation in which medication may be needed or a code situation in which one would follow hospital protocol External pacing may be an option for this patient Failure to Fire Pace In failure to fire or pace the patient s rhythm returns to whatever rhythm the patient had prior to receiving a pacemaker EKG Characteristics By definition this occurs when the pacemaker fails to create pacemaker spikes or it creates fewer than the preset number of pacemaker spikes per minute Nursing Priorities amp Potential Treatments When the patient returns to his pre pacemaker rhythm he will have a return of his pre pacemaker symptoms as well Like all bradycardic patients he will have hypotension possibly syncope or near syncope and chest pain His pre pacemaker rhythm may also be asystole In which case the patient will require emergent transcutaneous pacemaker possibly CPR and a code called Under sensing In under sensing a pacemaker spike will occur too soon after an intrinsic complex This occurs because the pacemaker did not see or sense the intrinsic beat When a pacemaker sees an intrinsic QRS or P wave it should inhibit and not fire The pacemaker should also reset its timer to the preset automatic interval to watch for the next intrinsic complex If the pacemaker does not see another intrinsic complex by the time its automatic
40. guide Nurses must make decisions about the patient s treatment based on information obtained from the electrocardiogram reading They must have the ability to read the data quickly so that they can begin medical interventions Bradycardia Symptomatic bradycardia Heart rate slower than normal for age or lt 60 normal age on pg with any signs of cardiac compromise altered LOC hypotension respiratory distress or failure poor cap refill Types of bradycardia Sinus bradycardia or AV block Treatment of Bradycardia CPR for HR lt 60 Maintain airway Oxygen EPI 0 1ml kg IV IO every 3 5 minutes first line drug for pediatric bradycardia Atropine 0 02mg ml IV IO for bradycardia caused by increased vagal tone or AV block Consider transvenous pacing Pediatric Bradycardia With a Pulse and Poor Perfusion Identify and treat underlying cause Maintain patent airway assist breathing as necessary Oxygen Cardiac monitor to identify rhythm monitor blood pressure and oximetry O IV access 12 Lead ECG if available don t delay therapy Cardiopulmonary compromise continues CPR if HR 60 min with poor perfusion despite oxygenation and ventilation Support ABCs Give oxygen Observe Consider expert consultation Epinephrine Atropine for increased vagal tone or primary AV block Consider transthoracic pacing transvenous pacing Treat underlying causes If pulseless arrest develops g
41. hrine theophylline Electrolyte abnormalities Myocardial ischemia or injury Digoxin toxicity Hyperthyroidism Other Types of PACs There are a few variations from the above description On occasion a PAC may not conduct into the ventricles or the PAC may conduct into the ventricles in an abnormal way Nonconducted PACSs If the PAC occurs very prematurely or close to the preceding T wave the early atrial depolarization might be too early for the right and left bundles to conduct the impulse This type of PAC cannot be conducted down into the ventricles In this situation look for an early P wave which might also be buried in the preceding T wave The early PAC does not conduct into the ventricles thus there is no QRS for this one cardiac cycle Aberrantly conducted PACs If the impulse should happen to travel abnormally through the ventricles the QRS may be prolonged This can happen if either the right or left bundle branches are not ready to depolarize and result in a temporary block If the QRS is wide following a PAC it will be called an aberrantly conducted PAC Nursing Priorities Intervention not typically required Heart rate may be irregular during episodes of PACs so assess the pulse for one full minute Potential Treatments Asymptomatic Observation and ECG monitoring for frequency and trends Explore potential underlying causes caffeine intake stress reduction myocardial abnormalities etc Symptomatic Treatment is typi
42. ht on time regular P to P intervals and the cycle of prolongation of PR intervals continues as the pattern is repeated The repetition of this pattern results in group beating e g three conducted sinus beats with progressively lengthening PR intervals and a fourth sinus beat that is NOT followed by a QRS Beats that are successfully conducted have a normal QRS width Because QRS complexes are periodically dropped the ventricular rhythm is irregular This block almost always occurs at the level of the AV node rarely at His bundle or bundle branch level is typically a transient rhythm and prognosis is good Causes Acute inferior MI right ventricular infarction increased vagal tone ischemic heart disease digitalis toxicity beta blockers amiodarone calcium channel blockers electrolyte imbalances rheumatic heart disease or myocarditis Nursing Priorities Check the patient s blood pressure and other patient vital signs often they are normal Assess the patient for possible causes Potential Treatment Most of the time this rhythm produces no signs and symptoms and requires no treatment If needed 2 degree Type I AVB will respond to atropine if the patient becomes bradycardic and hypotensive Temporary pacing should also be considered Find and treat reversible causes and observe for progression into higher forms of block 5 oo HL FH p E eee nt pus ie ppm M EE gcc
43. icular rate count the number of small boxes between two consecutive R waves and divide by 1500 To calculate the atrial rate count the number of large boxes between two consecutive P waves and divide by 1500 For example if there are two small squares between regular QRS complexes the heart rate is 75 1500 20 75 Quick Method used when rhythm is regular Find an R wave that falls on a thick vertical line and count the number of boxes until the next R wave The duration between two consecutive R waves 15 referred to as the RR interval Then use number range above counting down for each large box o Box 300 beats per minute bpm 2 Boxes 150 beats per minute bpm 3 Boxes 100 beats per minute bpm 4 Boxes 75 beats per minute bpm 5 Boxes 60 beats per minute bpm 6 Boxes 50 beats per minute bpm O O O O O 10 Basic EKG Rhythm Analysis Guide The ECG tracing provides a variety of clues as to what is happening within the heart These clues include heart rate regularity or irregularity of the rhythm interval measurements and characteristics of each individual waveform Think of the ECG strip as a unique fingerprint in which you are the detective conducting the investigation Like a detective you will need to pay attention to details In addition to a detailed analysis you will also need a recipe for ECG interpretation just like a cook needs a recipe for a complex dessert If you follow the interpretat
44. ing rhythm Causes Caffeine tobacco alcohol Digoxin toxicity Exercise Hypocalcemia Hyperkalemia New MI Proarrhythmic effect of antiarrhythmic agents Nursing Priorities Assess the patient s response Many patients are asymptomatic while others may feel palpitations or light headed Potential Treatments Treatment is required only when PVCs are frequent or the patient has intolerable symptoms Asymptomatic Observation Rule out hypokalemia and hypoxemia both can trigger PVCs Oxygen Correct electrolyte imbalances Symptomatic In the setting of an acute myocardial infarction PVCs indicate the need to aggressively treat the ischemia infarction with oxygen nitroglycerin morphine and potential antiarrhythmic agents 36 Ventricular Tachycardia rui me e 18 LEAD 11 1 EU E Ep Ec HI Hr Ur HA E s wr ei dE LEE CU ky VU c 1 Rate 100 250 BPM PRI P waves may be present if SA node is functional however there is no relation to the QRS It is unlikely that P waves will be visible since this rhythm typically moves at a very fast rate and the P waves will be buried in the QRS QRS Wide Bizarre gt 12 QT Rate dependant may be lt 40 seconds with a fast rhythm Difficult to differentiate between the QRS and the T wave Rhythm Ventricular rhythm regular Source of pacer Ventricular Purkinje Fibers
45. interval followed by one or more non conducted P waves The PR interval does not lengthen before a dropped beat Remember that the P waves that are successful in conducting through have a constant PR interval Since the SA node is firing in a regular pattern the P to P intervals again march through in a regular pattern P P is regular Since not all P waves are conducted into the ventricles the R to R intervals will be irregular and the ventricular response HR may be in the bradycardia range When the block occurs at the bundle of His the QRS may be narrow since ventricular conduction is not disturbed in beats that are not blocked If the blockage occurs at the level of the bundle branches conduction through the ventricles will be slower therefore creating a wider QRS complex gt 12 seconds Mobitz II is associated with a poorer prognosis and complete heart block may develop Causes are usually associated with an acute myocardial infarction severe coronary artery disease or other types of organic lesions in the conduction pathway The patient s response to the dysrhythmia is usually related to the ventricular rate The QRS complex is typically abnormal wider than 12 seconds due to the bundle branch block The block may be in a ratio of 2 1 two P waves for every QRS 4 3 3 2 Causes Can be caused by damage to the bundle branch system following an acute anterior AMI This is not caused by medications or increased vagal tone Nursing Pri
46. interval timer is completed the pacemaker will fire Remember a pacer spike tells you the pacemaker fired In under sensing you will see pacemaker spikes closer to the intrinsic complex than expected When it fires too soon the pacemaker is under sensing You will use the automatic interval to determine if the pacemaker is firing too soon EKG Characteristics Rate Pacer spike occurs too soon after intrinsic complex Extra spikes on EKG that are early Extra spikes may come in the middle of a P wave QRS or T wave Nursing Priorities amp Potential Treatments Palpitations Should the under sensing be occasional one should get a blood pressure pulse rate respiration rate and O2 saturation This is to determine if the patient 15 tolerating the under sensing If the under sensing is continuous the patient will be pulseless or have a symptomatic bradycardia This can range from a situation in which medication may be needed or a 45 code situation in which one would follow hospital protocol External pacing may be an option for this patient Over sensing In over sensing a pacemaker spike will not occur when expected We would expect the pacemaker to fire following its automatic interval when an intrinsic complex does not occur If the pacemaker does not see an intrinsic complex by the time its automatic interval timer is completed the pacemaker should fire Prior to completion of the second automatic interval an intrinsic complex occurred
47. ion recipe each time you analyze a strip your skills will grow and your interpretations will be consistently accurate Remember to print a 6 second strip or longer each and every time you begin an interpretation Follow the six basic steps your recipe for rhythm interpretation When looking at a cardiac rhythm ask yourself the following questions 1 Calculate heart rate Calculate both the atrial and ventricular rates Normally the atrial rate is the same as the ventricular rate Is this true in the ECG strip you are analyzing Remember the normal heart rate for most individuals falls between the range of 60 80 beats minute Normal Findings Abnormal Findings The HR should be between 60 80 Heart rates less than 60 beats minute are beats minute typically labeled as slow or bradycardic The atrial rate should be the same as the Heart rates greater than 100 beats minute are ventricular rate typically labeled fast or tachycardic 2 Regularity of the rhythm The assessment of the regularity of the rhythm Is the rhythm regular or is it irregular To assess the regularity you will need to place the legs of your calipers on two consecutive R waves This is your R to R or R R interval Without moving the width of the calipers march through the rhythm as you travel from R wave to R wave If you do not have calipers another method to determine regularity is to make a small mark on a piece of paper over two consecutive R
48. ionship between the P and the QRS waveforms The PR interval will be totally inconsistent and you may even see P waves superimposed in the middle of QRS complexes There will be more P waves than QRS complexes because the intrinsic rate of the sinus 32 node is faster than either the junctional or ventricular rates Since there is no connection between the atria and ventricles it is possible to have an atrial rhythm such atrial fibrillation or flutter and a junctional or idioventricular rhythm driving the ventricles This is illustrated in the EKG ini below i 5 ih ies Ez m mw HEHBA gt PTZ i mud bnt E F 7 EEG T 1 m Pm pu a L Causes 3 degree AVB may be transient and reversible or permanent Common causes are acute inferior or right ventricle MI ischemic heart disease in general increased vagal tone digitalis toxicity amiodarone beta blockers calcium channel blockers electrolyte imbalances Nursing Priorities Check the patient s blood pressure assess for syncope palpitations or SOB Your patient may need to lie down to prevent syncope and or potential falls Patient may have lower B P due to low ventricular rate Potential Treatment Asymptomatic Notify physician Observation and monitoring only Hold drugs that can slow AV node conduction Obtain supplies for pacing should this become necessary Symptomatic Notify physici
49. later Therefore if your rhythm 15 regular it cannot be atrial fibrillation Examine P wave First you must go on a P hunt and find the P waves Once you have identified them assess their characteristics Normal Findings P waves should be regular march out the P P intervals with your calipers P waves have a symmetrical shape usually upright and rounded P waves should all look alike uniform and should point in the same direction There should be one P for every QRS or a 1 1 relationship The QRS associated with P waves Measure PR interval Abnormal Findings A P wave 15 not followed by a QRS complex There are more P waves than QRS complexes completely dissociated The QRS complexes are completely dissociated from P wave Remember that the P to R interval represents the time it takes an impulse to travel from the atria through the AV node The P to R interval is measured from the beginning of the P wave to the beginning of the QRS complex This is a bit confusing as you might think it is a measurement from the beginning of the P wave to the beginning of the R wave but it is actually only measured from the beginning P to the beginning of the Q wave Think of it as a P to Q measurement despite fact that is called a PR interval Normal Findings The PR interval or time travel from SA to AV nodes 1s between 0 12 to 0 20 seconds The PR intervals are constant throughout the rhythm 12 Abnor
50. litude of pacemaker spike and a slowing pacemaker rate Pacemaker batteries will not run out unexpectedly When a battery is running low the elective replacement indicator ERI is activated Physicians can detect this activation during a routine office visit In addition the battery status and the general functioning of the pacemaker can be tested over the telephone This is generally done every one to two months Pacemakers will continue to function for approximately six months after the ERI is activated allowing ample time to schedule an elective replacement procedure Runaway Pacemakers Rapid rate of electrical impulse discharge results This potentially life threatening malfunction of older generation pacemakers 15 related to low battery voltage e g overdue pacemaker replacement The pacemaker delivers paroxysms of pacing spikes at 2000 bpm which may provoke ventricular fibrillation Paradoxically there may be failure to capture causing bradycardia because the pacing spikes are very low in amplitude due to the depleted battery voltage and because at very high rates the ventricle may become refractory to stimulation Application of a magnet can be lifesaving but definitive treatment requires replacement of the pacemaker Failure to sense Pacemaker fails to sense the patient s own intrinsic rhythm and generates a pacer spike in the intrinsic rhythm s own QRS absolute or relative refractory period of the T wave The ventricular 44
51. m mmmn e E NI EE x z RN E NE CEN mama Em mam m m EE Junctional Rhythm LUE SES HHI qs i i m RE Em er Tii M Pil 04 Rate 40 60 BPM PRI Absent or variable QRS Usually lt 12 may be wider depending on pacer site QT lt 40 may be prolonged with slower heart rates Rhythm Regular Source of pacer AV Node Junction Bundle of HIS Characteristics The AV node is a group of specialized cells and its main function is to delay impulses coming from the atria to ventricles thereby allowing the atria more time to completely contract Between the AV node and the right and left bundle branches lies the Bundle of His The area around the Bundle of His 15 also called the AV junction where the AV node and the bundles junction together This AV junction can function as a pacemaker It initiates impulses at a rate of 40 to 60 beats per minute Under normal circumstances the sinus node pacemaker 1s faster and predominates If the AV node 15 not depolarized by the arrival of a sinus impulse within approximately 1 0 to 1 5 seconds it will initiate an impulse of its own from this junctional area This 1s called a junctional escape complex It occurs because of failure of the sinus node to initiate an appropriately timed impulse or because of a conduction problem between the sinus node and the AV junction A repeated series of such impulses is
52. mal Findings The PR interval is gt 20 seconds this might indicate delayed travel time from SA to AV node The PR interval 1s irregular in measurement irregular or varying PR intervals may indicate some type of SA AV conduction problem and possible conduction heart block 5 Measure QRS Complex The QRS complex represents ventricular depolarization The QRS complex consists of three waves the Q wave the R wave and the S wave It is measured from the beginning of the Q wave to the end of S wave Normal ventricular conduction and depolarization takes no more than 12 seconds Normal Findings Abnormal Findings All the QRS complexes have uniformity The QRS complexes vary in shape width and throughout the same size shape and direction direction All QRS complexes are of equal duration or The QRS complex is gt 12 seconds wide width The R to R interval between each QRS is The R to R interval between each QRS is regular irregular 6 Examine ST segment should be isoelectric amp Examine T wave upright flat inverted spiked Normal Findings Abnormal Findings The ST segment should be electrically There is gt Imm ST segment elevation or neutral or near neutral and should be depression from the isoelectric line sitting on the isoelectric baseline no greater than mm above or below the isoelectric line is normal The T wave is upright whenever the R The T wave is in the opposite direction than the wave 15
53. nd basic ECG interpretation A six step process of rhythm identification has been taught as a framework for the interpretation of rhythms originating in the sinus junctional ventricular areas Heart blocks and life threatening rhythms have also been discussed Beyond interpretation all rhythms include nursing priorities and potential treatment strategies Every attempt has been made to provide information that is consistent with current literature including the American Heart Association guidelines Mastery of this complex topic requires several months to years of practice in the clinical setting Many first time learners need to re review sections of this module as their learning develops and when new questions arise 47
54. ntricular bigeminy is a when you see a pattern of one PVC then one normal beat then one PVC followed by a normal beat If every other beat is a PVC ventricular bigeminy is present If every third beat is a PVC the term Ventricular Trigeminy is used if every fourth beat is a PVC Ventricular Quadrigeminy is present and so forth The strip below is an example of ventricular trigeminy 7 o a Bote nn Keep in mind PVCs may occur as isolated complexes or they may occur repetitively in pairs two PVCs In a row When three or more PVCs occur in a row whether unifocal or multifocal Ventricular Tachycardia VT is present When VT lasts for more than 30 seconds it is arbitrarily defined as Sustained Ventricular Tachycardia R on T Phenomenon The T wave is a sensitive or vulnerable area in the cardiac electrical cycle Remember that the heart is now repolarizing and does not like to be stimulated at this time If an early ventricular beat comes in on top of or near the T wave the early beat could throw the heart into an uncontrollable repetitive pattern called ventricular tachycardia The term R on T phenomenon is used whenever an early ventricular beat lies near the vulnerable T wave Consult with MD if you see early R waves coming in near the T wave Early detection can help prevent your patient from developing a life threaten
55. o to Cardiac Arrest Algorithm 2010 American Heart Association 14 Cardiopulmonary Compromise Hypotension Acutely altered mental status Signs of shock Doses Details Epinephrine IO IV Dose 0 01 mg kg 0 1 mL kg of 1 10 000 concentration Repeat every 3 5 minutes access not available but endotracheal ET tube in place may give ET dose 0 1 mg kg 0 1 mL kg of 1 1000 Atropine IO IV Dose 0 02 mg kg May repeat once Minimum dose 0 1 mg and maximum single dose 0 5 mg Tachycardia Tachycardia Heart rate faster than is normal for the child s age Tachycardia with hemodynamic instability signs are altered LOC hypotension poor cap refill weak pulses respiratory failure Sinus tachycardia fast rate depending on age amp varies with activity HR lt 220 infants HR lt 180 children Treatment identify amp treat possible causes hypovolemic shock fever anxiety toxins SVT Does not change with activity Common symptoms are irritability rapid respirations poor feeding poor cap refill pallor hypotension and diaphoresis HR gt 220 infants HR gt 180 children Pediatric Tachycardia With a Pulse and Poor Perfusion Identify and treat underlying cause Maintain patent airway assist breathing as necessary Oxygen Cardiac monitor to identify rhythm monitor blood pressure and oximetry O IV access 12 Lead ECG if available don t delay therapy
56. orities Check the patient s blood pressure Assess the patient s symptoms Note Mobitz II has the potential to suddenly progress to complete heart block or ventricular standstill have a temporary pacemaker nearby Potential Treatment Asymptomatic Observation and monitoring only Hold drugs that can slow AV node conduction Notify physician Obtain supplies for pacing should this become necessary Symptomatic If symptomatic bradycardia is present apply transcutaneous pacemaker and collaborate with physician for insertion of transvenous pacer wire Administer a dopamine infusion if patient is hypotensive Note Atropine must be used with great caution if at all with this rhythm Atropine will increase the sinus note discharge but does not improve conduction through the AV node the location of this block is lower in the conduction system Acceleration of the atrial rate may result in a paradoxical slowing of the ventricular rate thereby decreasing the cardiac output 31 3rd Degree AB Block Complete Heart Block k 12 66 GSMAYG S LEAD II 1 6 Rate Atrial rate is normal Ventricular rate is slower 40 60 bpm if back up pacer is from the junction or 20 40 bpm if back up pacer is from the ventricles PRI No relationship between P waves and QRS complex QRS Width 12 seconds if controlled by the junction gt 12 seconds if paced by the ventricle QT May be lt 40 seconds if it is a junctional rhythm or may be wider gt
57. output or blood pressure The terms coarse and fine have been used to describe the amplitude of the waveforms in VF With Coarse VF the fibrillatory waves are more easily seen and are usually greater than 3mm in height 3 small boxes tall Coarse VF usually indicates a more recent onset of VF which could be more easily converted by prompt defibrillation The presence of fine VF which looks a bit like asystole and is less than 3mm in height often means there has been a considerable 9 since collapse and successful resuscitation 15 more difficult r IALL im en LALI L labia T Hit AA p idi pul Be Gena p pL ae Eid k Tok tall ES dl H WA VIDEAR ee zur MAN cas Wy AV AP BEC i ru E HE HR PHH s Causes CAD AMI trauma hypoxia acidosis antiarrhythmics electrolyte imbalances cardiac catheterization cardioversion accidental electrocution cardiac pacing and extreme hypothermia Nursing Priorities Check for an airway breathing and pulse per Basic Life Support BLS standards Call for help The patient will be apneic pulseless and unresponsive Begin CPR VF treatment requires electrical therapy defibrillation Resuscitation requires defibrillation and often requires emergency drugs per ACLS VF guidelines The sooner the patient is defibrillated the more likely of achieving spontaneous circulation The longer the patient is
58. phrine nipride and caffeine Sinus Tachycardia increases the hearts need for oxygen decreases ventricular diastolic time and decreases coronary artery perfusion Reflexive Sinus Tachycardia is often seen in hypotensive patients in an attempt to maintain adequate blood pressure Nursing Priorities Check your patient s blood pressure assess for syncope palpitations or SOB Patient may need to lie down to prevent potential falls Patient may have lower B P due to decreased diastolic ventricular filling time associated with the tachycardia Potential Treatment Asymptomatic Observation Symptomatic Treat the underlying cause dehydration anxiety etc Drugs such as beta blockers may be given to slow the HR The underlying cause must be identified and treated Drugs that may be given to slow the heart are digitalis beta blockers calcium channel blockers sedatives and various other antiarrhythmic medications EEE EEE EHIH SSS c ppt pt p OE EOS E do UU SAT A RAE ARI ARA AAT S b Rl ala IRE HS Qe EE UR eae eee RU UE ERE SE EE FERE ESTE tie are ee qd ete HHHHH pH RN RN D E d D DD DIN Supraventrical Tachycardia 1 a a mama H k b 1 Sete PIN BOATUO PSVT Rate gt 150 BPM PRI Usually lt 12 sec QRS Narrow lt 12 sec QT lt 40 sec Rhythm Regular Sou
59. r pulseless VT Notify physician Treatment depends on the patient s response to the VT rhythm Potential Treatments Asymptomatic or stable Oxygen obtain 12 lead ECG consider Lidocaine or Amiodarone Check electrolytes such as potassium and magnesium Apply multifunction pads as cardioversion may be necessary if patient becomes unstable Symptomatic If unstable prepare for immediate synchronized cardioversion Consider amiodarone bolus and infusion If pulseless administer one defibrillation shock followed by CPR Activate your code resuscitation team and follow ACLS guidelines 37 Ventricular Fibrillation Rate Unable to measure due to rapid and uncoordinated electrical activity P waves None PRI None QRS None QT none Rhythm Rapid and chaotic No discernable rhythm Source of pacer Multiple sources of ectopy in the Ventricular Purkinje Fibers Characteristics Ventricular fibrillation VF is the result of highly irritable ventricle s which begin to send out rapid electrical stimuli The stimuli are chaotic resulting in no organized ventricular depolarization The ventricles do not contract because they never depolarize For you visual learners just imagine shaking a bowl full of Jell O Gently shake the bowl and watch the Jell O quiver or fibrillate This is similar to what is happening within the heart Because the ventricles are fibrillating and never contracting the patient does not have a pulse cardiac
60. rce of pacer Atrial re entry current Characteristics Tachycardias with a narrow QRS lt 12 seconds and faster than 150 BPM do not originate from the SA Node since the upper limit rate for the SA NODE is 150 The rhythms can vary in name from Supraventricular Tachycardia SVT Atrial Tachycardia or a rhythm that may speed up and slow down called Paroxysmal Atrial Tachycardia or Paroxysmal Supraventricular Tachycardia If P waves are visible the rhythm may be called Atrial Tachycardia if no P waves are visible due to a very fast rate label the rhythm SVT The onset of PSVT PAT is typically abrupt with the onset being initiated by a premature atrial beat The arrhythmia may self terminate in a few minutes to a few hours Nursing Priorities Check your patient s blood pressure assess for syncope palpitations or SOB Patient may need to lie down to prevent potential falls Patient may have lower B P due to decreased diastolic ventricular filling time associated with the tachycardia Potential Treatment Asymptomatic Observation Symptomatic Cardioversion Carotid sinus massage Valsalva maneuver IV adenosine IV Verapamil Oral anti coagulants for stroke prevention Identify and treat cause Premature Atrial Contractions PACs Rate Typically normal Rhythm Underlying rhythm is typically regular with early premature beats P waves Atrial depolarization is premature occurring before the next normal P wave Since the impul
61. referred to as a junctional escape rhythm P WAVE P WAVE BURIED IN QRS WAVE MAY BE ABSENT P WAVE AFTER QR5 Unusual or Absent P waves If the AV junction paces the heart the atria may or may not be stimulated The electrical impulse must travel in a backward retrograde direction to activate the atria In Leads II and aVF the P wave will be negative inverted if the atria are stimulated Depending on how the atria responds to the junctional pacemaker the patient could have a no P waves b an inverted P wave upside down just preceding the QRS or c an inverted P wave after the QRS if atrial depolarization occurs after the QRS Causes Electrolyte imbalance sick sinus syndrome digitalis toxicity interior wall MI rheumatic heart disease hypoxemia Nursing Priorities Check your patient s blood pressure assess for syncope palpitations or SOB Lower blood pressure may result from loss of atrial kick and bradycardic Potential Treatments Observation Find and treat reversible causes temporary or permanent pacer atropine 0 5 1 0mg may cause the SA Node to overdrive the AV Node and increase the heart rate Treatment is only needed if the ponens is p or Bae instability cem 181 HH HH I Accelerated Junctional Rhythm Junctional Tachycardia Accelerated Junctional Rhythm Rate 60 100 bpm Remember
62. se originates outside the SA node the P wave may have a different shape often notched peaked or buried in the proceeding T wave PR Interval Maybe normal shorter or longer than normal PR interval depending on origin of the PAC QRS Width typically normal but may be prolonged if the PAC is aberrantly conducted through the ventricles Characteristics The intrinsic pacemaker of the heart is the sinus SA node and normally it initiates each beat Pacemaker stimuli can also arise from other parts of the heart the atria the AV junction or the ventricles The terms ectopy or ectopic beat are used to describe these non sinus beats Ectopic beats are often premature that is they come in early or before the next sinus beat is due A premature atrial contraction results from an ectopic stimulus that arises from somewhere in either the left or the right atrium but not in the sinus node The atria are depolarized from the ectopic stimulus but the remainder of the conduction is typically normal through the AV Node Junction and downward into the bundle branches i e normal PR and QRS morphology and intervals Possible Causes PACs are very common and may occur in persons with a normal heart or in persons with virtually any type of organic heart disease PACs do not imply that a person has cardiac disease and may be seen with caffeine intake and with emotional stress Other causes include Administration of sympathomimeticagents epinep
63. smia You will need to be able to recognize the four lethal rhythms Asystole Ventricle Tachycardia VT Ventricle Fibrillation VF and Polymorphic Ventricle Tachycardia Torsade de pointes Use this study guide and other resource books to review ECG interpretation You will be expected to calculate rates properly interpret each strip Practice measuring your strips in the study guide The rhythm strips on the exam are NOT 6 second strips Use calipers or the attached handout to determine rates Memorize your blocks there are several rhythm strips on blocks Rules for passing the exam Minimal passing score 85 If you do not correctly identify any of the following rhythms you will be required to retake the exam even if your test score is above the passing score o Ventricular tachycardia o Ventricular fibrillation o Asystole o Torsade de pointes If you correctly identify the four lethal rhythms and achieve an overall score of at least 85 you have passed the exam For Information Purpose Only The 2010 ECC Adult algorithms for cardiac arrest bradycardia with a pulse and tachycardia with a pulse are included in this study guide Changes have occurred with the 2010 guidelines so please take time to review the following link http guidelines ecc org pdf 90 1043 ECC 2010 Guidelines Highlights noRecycle pdf Questions Give us a call Larry Lybbert RN BSN MS Angela Stone Banner Staffing Services Banner Staffing S
64. t reversible causes Overdrive pacing with the use of an external pacer or Isuprel may overdrive the ventricular rate and break the triggering mechanism of the arrhythmia Magnesium sulfate may also be effective Refer to your ACLS manual for detailed treatment algorithms Polymorphic ventricular tachycardia with a pulse requires defibrillation not synchronized cardionversion 40 Al Idioventricular IVR SH HiHi HHH Ey H pH HA HEH Fr EE HH EE ES IE EH HE HEHEHHEESEHEHEHHEHHHEHHTHHEHHEHHEHHEHHHYEHHHSHHHE EHEH p Rate 20 40bpm PRI absent since the electrical activity is coming from the ventricles QRS Greater than 0 12seconds Wide and bizarre Characteristics Normally the pacemaker of the heart that is responsible for triggering each heart beat ventricular contraction is the SA Sino Atrial node However if the ventricle does not receive triggering signals at a rate high enough the ventricular myocardium itself becomes the pacemaker escape rhythm This is called Idioventricular Rhythm Ventricular signals are transmitted cell to cell between cardiomyocytes and not by the conduction system creating wide sometimes bizarre QRS complexes gt 0 12 sec The rate is usually 20 40 bpm If the rate is gt 40 bpm it is called accelerated idioventricular rhythm The rate of 20 40 is the intrinsic automaticity of
65. tion of the hearts cells The EKG waveform consists of Wave Represents atrial depolarization QRS Represents ventricular depolarization T Wave Represents ventricular repolarization Intervals are described as the length of time between one waveform and the next Isoelectric Line Flat line of the EKG tracing represents no electrical activity and is referred to as the baseline Deflections above the isoelectic line are positive and deflections below the isoelectric line are negative P Wave The SA node produces an electrical stimulus the P wave normally upright usually no more than 3mm in height PRI PR Interval Is representative of the spread of the atrial depolarization wave and the time it takes for the impulse to conduct through the AV node and to the ventricles The PRI is marked from the start of the P Wave to the beginning of the QRS The PRI is normally no more than 0 20 seconds in length QRS Complex The QRS represents depolarization of the ventricles and ventricular conduction time of the electrical impulse Typically the QRS is narrow with a conduction time of no more than 0 12 seconds The QRS is measured from the beginning of the first waveform to the point at which the waveform returns to the isolectric line The QRS 15 made up e Q Wave First negative deflection from baseline below the isoelectric line R Wave Positive deflection from the baseline above the isoelectric line S Wave Neg
66. upright The T wave deflects R wave downward when the R wave is downward Rhythm Interpretation Believe it or not after completing Step 6 you are ready to make an educated decision on naming the correct rhythm Remember to correlate information obtained in Steps 1 6 along with your understanding of the heart s electrophysiology Rather than pure memorization if you can integrate the electrophysiology with the rhythm interpretation your patient care priorities and potential treatments will make a lot more sense Six Basic Steps for Rhythm Interpretation Summary Rate Calculate the heart rate HR or note the HR from the Regularity Measure the regularity or rhythm of the R waves P wave Examination Is there one P wave before each QRS there should be P to R interval Measure the P to R interval Is it within normal limits It is consistent QRS width Measure the duration of the QRS complex Rhythm interpretation 13 Nursing Priorities and Potential Treatments Pediatrics Nurses Required All Other RNs Informational Only Interpreting the actual ECG rhythm is only the beginning of the assessment and care for your patient You cannot be successful in your practice if you only know how to interpret ECG As healthcare provider you must be able to respond with appropriate priorities and understand initial treatments Complete comprehensive treatments for each type of ECG rhythm are beyond the scope of this review
67. ventricie 7 branches QqRs complex T wave 34 Premature Ventricular Contraction PVCs i 4 i i MB 226 Boos r i z 5 EERE TETEE ees pe IPL boc R i i et Goes Rate Depends on the underlying rhythm Rhythm Depends on the underlying rhythm The PVC beats are premature so this will make the R to R interval a bit irregular P waves Not applicable there are no P waves associated with PVCs PR Interval Not applicable QRS Width gt 12 seconds wide and bizarre in appearance T wave may be opposite direction of QRS complex Characteristics A premature ventricular contraction PVC is a depolarization that arises in either ventricle before the next expected sinus beat and 1s therefore labeled premature They are generally easy to detect because the QRS is wide and bizarre looking Since PVCs originate in the ventricle the normal sequence of ventricular depolarization is altered For example instead of the two ventricles depolarizing simultaneously a PVC will cause the ventricles to depolarize at different times or sequentially In addition conduction occurs more slowly through the myocardium than through specialized conduction pathways This results in a wide 0 12 second or greater and bizarre appearing QRS The sequence of repolarization is also altered usually resulting in an ST segment
68. waves then move the paper to the next R wave and see if the dots line up march out Do the R waves follow a regular pattern If so the ventricular rhythm is called regular rhythm Normal ECG rhythms are regular in their pattern If the R R interval varies in the number of ECG small boxes between them you are dealing with an irregular rhythm Do the same type of assessment with the atrial rhythm Put your calipers at the beginning or upslope of a P wave Put the other end of your caliper at the beginning of the next P wave or make a small mark on a piece of paper over two consecutive P waves This 15 P P interval Lift your calipers and begin marching through the strip looking for the pattern of regularity of the P waves If the SA node is firing at a constant beat the P P interval will be regular Do not estimate Use an EKG caliber or paper 11 3 4 Normal Findings The R R intervals are regular The P P intervals are regular There is one P for every QRS Regular rhythm Abnormal Findings The R R intervals are irregular The P P intervals are irregular There is more than one P for each QRS Irregular _ HEHEHHHHHHH SSS SSeS 076495 See PRESS Peres Thea II 41 OGOS 000606 606065 66505 606565 66 500 6 ioi ottoedototdrtrido top tt gg Very few rhythms are irregular For example atrial fibrillation 1s always irregular more on this rhythm
69. wed by a pause without QRS complexes 1 1 conduction may recur or may progress to ventricular asystole or complete heart block PR interval remains constant until a block occurs and the QRS complex is dropped resulting in a pause When or if conduction resumes the PR interval remains constant Normal if block is at level of bundle of His Wide 20 12 s if block in bundle branches Yes QRS QRS rate is constant until a QRS complex is dropped and a pause occurs b Images of second degree and complete heart block are reprinted from Huszar 19 with permission Copyright Elsevier 2002 28 Atrial rate and ventricular rate are always different atrial is faster than ventricular Regular with ventricular rate slower than atrial Rate May become irregular as heart becomes ischemic P to P wave is constant but P waves may be difficult to see if buried in the QRS complex or T wave Variable more P waves than QRS complexes PR interval is not consistent Impulses are not conducted from the atria to the ventricles Visually the PR interval is not constant and does not progressively lengthen no pattern Normal or wide Normal 0 12 s if block at level of atrioventricular node or bundle of His Wide 20 12 s if block in bundle of His Ist Degree AV Block os 1 bu Li Beda a Ng ee PER BGE Wes fed i Hmm ied ie 0 LE
70. ystem Generator controls rate amp strength of each electrical impulse Lead wires electrode at the tip relay the electrical impulse from the generator to the myocardium Types Temporary used to sustain HR in an emergency situation Transcutaneous TCP external cardiac pacing Transvenous lead wire threaded through the skin into a large vein Indications Suppression of ectopic atrial or ventricular rhythm Acute MI with symptomatic bradycardia 2 amp 3 degree AV block or bundle branch block Maintenance of adequate HR during special procedures or as prophylaxis after an open heart surgery Termination of AV nodal reentry Permanent implanted in patient s chest Indications Chronic atrial fibrillation with slow ventricular response Fibrotic or sclerotic changes in the cardiac conduction system Sick sinus syndrome or Sinus node dysfunction Tachyarrhythmias Symptomatic bradycardia and Third degree AV block not responding to pharmacologic interventions Atrial lead wire inserted into the Right atrium stimulates the atrium then travels down the electrical conduction through the ventricles err SSNS eben e t THILILLHM Ventricular lead wire inserted into the Right ventricle The electrical impulse from the pacemaker generator produces ventricular depolarization ANZ NAN NL ENAR RUBER NONI a TI 43 AV sequential two electrodes

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