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ER Club EKG Interpretation

Written by Henry Feld an! "#$

Re%ie&ed by Mariano Rey! M'! "()

This page will help you learn to interpret 12-lead EKG patterns. This is not a comprehensive guide to EKG interpretation, and for further reading, Dubin is the introductory boo of choice. !lease refer to the EKG tracing below if you are not familiar with the labeling of the EKG waveforms.

Step $

* HEART RATE )

The first step is to determine the RATE, which can be eyeballed by the following techni"ue. #ocate the $%& (the big spike) comple' that is closest to a dar vertical line. Then count either forward or bac wards to the ne't $%& comple'. (or each dar vertical line you pass, select the ne't number off the mnemonic )*++-1,+-1++--,-.+-,+) to estimate the rate in beats per minute /0!12. 3n other words if you pass 2 lines before the ne't $%&, the heart rate /4%2 would be less than 1,+. %emember that this is merely an estimate. 5ou should use real measurements to determine the e'act 4% /for precise measurement6 each large bo' represents 2++msec and small bo'es represent 7+msec2. 8s an e'ample of using the mnemonic, in the segment of the EKG below, start at the $%& that lines up with the vertical line at )+). 9ow counting bac each vertical line to the previous EKG )*++-1,+-1++) we notice the 4% to be slightly less than 1++ /probably around :+-:,2.

Step +

* RHYTHM )

9e't we need to determine the RH,THM both its source and its regularity. The prime concern is whether the source of the rhythm is the &8 node /sino-atrial2 or an ectopic pacema er. To determine whether the source of the rhythm is )sinus) or an ectopic rhythm, you need to loo at the relationship of the !-wave, if present, to the $%&-comple'. 3f there is a ! wave before each $%& and the ! is in the same direction as the $%&, the rhythm can be said to be sinus. (or instance note in the EKG segment below that there is a !-wave before each $%& /highlighted in blue2 and that it is pointing up as is the $%& segment.

8lso loo at the "uality and "uantity of !-waves before each $%&. There should only be one !-wave before each $%&. The !-wave should be in only one direction, and not biphasic /e'cept for leads ;1 and ;22. 3t should also be closer than 2++ms to the $%&. The shape of the !-wave should also be gently rounded and not pea ed.

Step -

* AXIS )

9e't we need to determine the A.IS of the EKG tracing. To do this we need to understand the basic . leads and their geometry. The EKG waveform comes from a measurement of surface voltages between 2 leads. 8 wave that is travelling to&ard/ the positive /<2 lead will inscribe an upwards deflection of the EKG= conversely a wave traveling a&ay from the positive lead will inscribe a downward deflection. >aves that are traveling at a 0# de1ree an1le to a particular lead will create no deflection and is called an i/oele2tri2 lead. 8s an e'ample in the pictures below, a wave travelling from the head to the feet would be shown as an upwards deflection in 8;(, since it is going towards the 8;(< lead. The a'is is the sum of the vectors, produced by the e g leads, to produce a single electrical vector. %emember that a positive signal in #ead-3 means that the signal is going right to left= this produces a vector, which if we ta e all the leads, we can sum. This summed vector should in general be pointing the same direction /down-left2 for a normal heart= this ma es sense if we thin of the electrical conduction system of the heart which sends a signal from the &8 node /top right2 to the pur in?e fibers /bottom left2. @onAt worry if you still donAt get it, weAll give you a visual e'ample further down the page.

Blic here to view the 0asic . #imb EKG #eads in *@ 5ou will notice that leads 3, 33 and 333 form the sides of an e"uilateral triangle, while 8;%, 8;# and 8;( bisect the vertices of the triangle. The easiest way to figure out the a'is is to draw a normal C-5 graph and fill in the "uadrants that are represented by each lead with a positive deflection. There are some tric s to save you time, but first thin about a normal EKG plot= in a normal EKG both leads 3 and 8;( will be positive as the signal travels from the &8 node /top right of the heart2 to the tip of the ventricles /bottom left of the heart2. This is a normal a'is, and leads us to the rule of thumb, if 3 and 8;( are positive the a'is is normal. 4owever, ?ust because this is not the case does not mean that the a'is is

* abnormalD /5ou need to loo at more leads in this case2 The normal a'is actually allows the signal to travel up to *+E above the C-a'is and *+E to the left of the 5 a'is. #etAs loo at an e'ample below and prove this.

3f the a'is is not completely in the bottom left /the patientAs left2 "uadrant /i.e. 3 and 8;( are positive2, it is simply a matter of using additional leads to determine the a'is. #oo ing at the map of all the leads, we notice that almost *.+ degrees of a'is are covered. Fse the same a'is determination method you used with 3 and 8;(.

Step 3

*LEAD POSITION4

Fnderstanding the precordial leads and how they align with the heart is critical to understanding the EKG. (irst letAs remember how the heart is located in the chest. 9ote that it sits flat above the diaphragm on the left side of the chest, and is pointed slightly to the left. This is important in understanding how the precordial leads correlate to the actual heart anatomy. >e see below the precordial leads in their relationship to the heart and chest anatomy.

Blic here to view the !recordial #eads in *@ ;1-;2 are over the right ventricle, while ;7-;. primarily are over the left ventricle. ;* is a transitional lead, and is appro'imately over the intraventricular septum, so it covers some of both ventricles. %emember that the bul of the left ventricle is posterior, so feel free to create a ;- and ;G to get more information of the left ventricle.

Step 5

/Hypertrophy)

7 4ypertrophy is the increase in siHe of the myocytes in the myocardium, leading to thic er walls. 3t can be non-pathological, as in the case of people who fre"uently perform isometric e'ercise /lifting heavy weights, with the straining and valsalva maneuver, produces an increased afterload2. E'tending this thought, we can see how hypertrophy can occur in the pathological sense by thin ing about increased afterload on the heart as in individuals with high blood pressure that causes a left sided afterload increase. #eft &ided afterload increases, such as systemic hypertension or aortic stenosis will cause the left ventricle /#;2 to e'pand in response giving #eft ;entricular 4ypertrophy /#;42. The right side of the heart can also e'perience afterload. 3ncreased pressure in the pulmonary vessels will cause an increase in afterload /bac pressure2 to the right ventricle /%;2, leading to an increase in muscle mass of the %; to compensate, leading to %ight ;entricular 4ypertrophy /%;42. 8s the ventricles, the atria can also become hypertrophic /dilated2, which is visualiHed as changes to the !wave. The !-wave can become biphasic in bilateral atrial hypertrophy. The best place to loo for 8trial 4ypertrophy is in ;1, which is mostly over the right atrium, but being the highest placed lead in the chest also gives left sided information as well2. 0elow we see e'amples of %ight and #eft 8trial 4ypertrophy showing as biphasic !-waves.

9e't we need to e'amining the ventricles for evidence of hypertrophy there. &ince increased muscle mass, logically yields to an increase in the signal /more channels -I more current2 we would e'pect to see changes in the $%& comple' morphology. (or %ight ;entricular 4ypertrophy we loo at ;1 /and less so in ;2 and ;*2 and notice that there is a large %-wave /the normal ;1 has a small % with a large &2

This increased % height, will taper down, in ;2 and ;*. %emember that ?ust because you find %;4 doesnAt mean that the left ventricle is al/o not hypertrophied, in which case you may not see the normal taper. 3n #eft ;entricular 4ypertrophy /#;42, you will have a large & wave in ;1 and a large % wave in ;,. The actual criteria, are to add the height of & in ;1 and the height of % in ;, /in mm2 and if the sum is greater than *,mm, then #;4 is probable. (or instance in the picture below, we measure the heights /2*mm in ;1 and 1-mm in ;,2 which total greater than *,mm, so we meet a criterion for #;4.

Step )

*BLOCK4

, 8 bloc is an interruption of the normal flow of an electrical impulse traveling down from the &8 node to the ventricles. The bloc s can occur in the &8 and 8; nodes as well as in the bundles. SA 6ode Blo27 consists of a failure of the &8 node to transmit an impulse, and is usually seen as a complete pause of 1 beat /i.e. a )s ipped beat)2= if the pause lasts longer or the morphology of the ! wave before and after the pause is different, it probably isnAt &8 bloc . This bloc can occur occasionally in normal patients, and should not necessarily be viewed as pathological. 4ere is an e'ample of &8 node bloc 6

A8 6ode Blo27 is a bloc which delays the electrical impulse as it travels between the atria and the ventricles in the 8; node. &ince the !-wave represents the activity of the &8 node, and the $%& comple' represents the activity of the ventricles, it ma es sense that the !-% interval represents the delay through the 8; node. The criteria for 1E 8; node bloc is a !% interval greater than .2 seconds /2++ms or 1 large bo'2. 0elow we see an e'ample of 1E 8; node bloc .

1E 8; 0loc - !% 3nterval I 2++ms +9 A8 Blo27 is where there are more than 1 !-wave preceding each $%& comple'. The !-waves are spaced in a regular rhythm, but there is no following ventricular response. >e see this below where there is a 261 ratio of !-waves to each $%&. 9ote that other ratios do occur /*61, 761, etc...2

2E 8; 0loc with a 261 !-wave ratio -9 Blo27 is a complete bloc of signals from the atria to the ventricles. 8s such we would e'pect complete dissociation between the timing of the !-waves and the $%& comple'es. The !-waves will be in a normal sinus rate, while the $%&As will be either in a nodal rhythm /.+bpm2 or a %entri2ular rhythm /*+-7+bpm2. 4owever, the ey is the lac of synchroniHation between the two. The lac of synchroniHation is what determines whether you are in a 2E 8; bloc with a greater than 161 ratio or *E bloc . 3t is important to e'amine the morphology of the $%& comple'= if it is a narrow comple', then the origin is li ely to be nodal, while a wide comple' is li ely to be ventricular, although one should also ta e the rate into account. 0elow we see an e'ample of *E 0loc with a narrow $%&= note the dissociation between the !-wave rate and the $%& rate.

*E 0loc Bundle Bran2: Blo27/ /002 are bloc s within the ventricular bundles, and normally consist of a left or right bundle branch bloc . 5ou will often hear these erroneously referred to simply as a left or right "bundle", the )block) being superfluous. The bloc s can be of the entire ventricular bundle or a fasicle of a given bundle. 4ere, we are simply going to introduce basic bundle bloc s. The ey to recogniHing a bundle bloc is to find a R;R" wave= the 2 % waves per comple' are really 2 superimposed $%& comple'es from each of the ventricles firing separately but very close in time to each other. The criteria consist of a $%& wider than .12 seconds /*mm2 and the 2 % waves. 3n a left bundle bloc , the left ventricular firing is delayed, while in right bundle bloc , the right ventricular firing is late. 0elow we see e'amples of %ight and #eft 0undle 0ranch 0loc s. 9ote the %-%A comple' repeating as well as the $%%& comple' being wider than *mm /.12sec2. 3n the %ight 000, the % wave represents the #eft

. ;entricular depolariHation, while the %A wave represents the delayed right ventricular response. 3n the #eft 000, the % wave is the right ventricle and the %A is the left ventricle.

%ight 0undle 0ranch 0loc /#ead ;12

#eft 0undle 0ranch 0loc /lead ;,2 %emember to consider what precordial lead the bloc is presenting in= if the bloc morphology presents best in ;1-;2, then it is a %ight 000, while a #eft 000 pattern is best appreciated in leads ;,-;.. 9ote6 the a'is will be hard, if not impossible, to accurately determine, as the ventricles are firing asynchronously with each other, altering the normal interventricular phasing.

Step (

Ischemi ! I"# rct "$ I"%&ry

Bardiac 3schemia and infarctions are the most important acute EKG patterns to detect. >e will deal with the li<e t:reatenin1 arrhythmias, such as 8systole, ;-(ib and ;-Tach in the ne't section as they are radically different from normal EKGAs, and should be handled separately. >hen a patient presents to the E% with chest pain, it is important first to immediately perform a 2o plete EKG analysis with the preceding steps, unless a life-threatening rhythm is detected, along with the physical e'amination and clinical assessment of the patient. I/2:e ia is when blood flow to the myocardium is insufficient to maintain the metabolic demand of the myocytes. 3schemia can present with symptoms ranging from mild chest discomfort on e'ertion to the most severe form of ischemia, which results in the crushing chest pain of a infarction= 3schemia may also be silent.

The %ange of !erfusion of the 1yocardium &urprisingly, the $%& is not the most affected part of the EKG waveform in ventricular ischemia. The &T segment is most often affected in ischemic conditions. >e will e'amine the 2 types of &T-segment changes6 ele%ation and depre//ion. These usually represent transmural ischemia and subendocardial ischemia respectively.

Tran/ ural I/2:e ia

The hallmar of acute transmural ischemia /across the heart wall from endocardium to epicardium2 is the elevation of the &T segment of the EKG. This is visualiHed by the &T-segment being raised above the isoelectric baseline. This change in the &T segment is mostly localiHed in the lead most directly overlying the ischemic myocardial area.This is due to a higher /more positive2 resting voltage of ischemic cells, which cause the &T-segment baseline to be more positive /an upwards deflection2. This change in the &T segment is mostly localiHed in the lead most directly overlying the ischemic myocardial area. The etiology of transmural ischemia is the blood supply failing to feed the myocardium. This may lead to un/table an1ina, and should be ta en very seriously, as this is the condition that progresses to an a2ute MI. 8s the ischemia becomes more e'tensive the &T segment elevation becomes more pronounced. The lead in which the &T elevation appears, allows you to accurately locate the ischemic or infarcted area of ventricular myocardium. 3f the elevation appears in inferior leads, this indicates an inferior ischemicJinfarcted myocardium= the lateral leads, li ewise indicate lateral wall ischemiaJinfarction.

&T-&egment Elevation 3t is important to differentiate pathologic &T segment elevation from non-pathologic =;point elevation. Kpoint elevation is identified by an elevation of the terminal portion of the $%& which then dips bac down towards the baseline before rising bac up to the &T segment. This is opposed to the pathological &Televation which is visualiHed as the terminal portion of the $%& going directly up to the T-wave.

K-!oint Elevation 8fter the ischemia has progressed to an infarct, and the tissue has scarred, the EKG will show an in%erted T &a%e. 8 pronounced >;&a%e /not normally present2 and loss of all or part of the % wave may also present.

$-waves with 3nverted T->aves

Sub;Endo2ardial I/2:e ia
#etAs loo at the progression of ischemia in the subendocardium. %elative decreased flow in the subendocardial regions is a normal conse"uence of the s"ueeHing of the myocardium, which compresses the blood supply to the endocardium during ventricular systole. 4owever, this can also be a pathological condition, e'pressed in /table;an1ina. This is a condition where the myocardial demands e'ceed the coronary artery blood supply /as opposed to unstable angina which is a supply problem2. This is represented on the EKG as &T-segment depre//ion. >ith ischemia of the subendocardium the ischemic cells become more positive in their resting voltage /due to channel lea age2 and this ma es the subendocardium more positive= since the endocardium is further away from the precordial leads than the more negative mycardium we see this as a depression /see figure below2. from Fnli e elevation, the &Tsegment depression is not localiHable to a specific lead, but is seen in the leads with the tallest % waves, which are the inferior leads /33, 333 and 8;( and leads ;7-;.2. Typically, stable angina will self-resolve, however, li e elevation, the depression is increased as the myocardial demand increases. 0elow we see an e'ample of &T-segment depression.

&T-&egment @epression in subendocardial ischemia

Step ?
Mi/2ellaneou/
This section will deal with the miscellaneous rhythms that can present often as life threatening arrhythmias, however they donAt fall into the simple categories outlined in the previous pages.

8entri2ular Fibrillation
;entricular (ibrillation /often called 8;Fib2 is the most life threatening arrhythmia, and is often the end rhythm before the a/y/tole of death. The physiology of this rhythm, is a complete brea down in the synchroniHation of the myocardial conduction system= different areasJcellsJsegments of the heart, are contracting and rela'ing with no coordination with other parts. This random "uivering results in a loss of cardiac output, resulting rapidly in death if untreated. The EKG pattern of ;-(ib is recogniHed by a total lac of organiHed activity, ranging from 2our/e /large amplitude2 to <ine /close to asystole2 in amplitude. The only )cure) for ;-fib is electrical cardioversion /defibrillation2. 4owever, before cardioverting a patient, remember to assure yourself, that this is actual cardiac activity, and not an artifact of patient movement /such as a seiHure, shivering or !ar insonAs disease2, electrical interference or other artifacts. 0elow are e'amples of course and fine ;-(ib.

Bourse and (ine ;entricular (ibrillation

Ta2:y2ardia
#i e any other heart rhythm the origin of the signal can be either atrial or ventricular. The source of a tachycardia, if ventricular, is always pathologic, while non-ventricular tachycardias can be thought of as )sinus) and supraventricular /&;T2 rhythms, and may or may not be pathologic. !athologic tachycardias can arise from multiple causes, such as an ectopic pacema er cell which we call abnormal automaticity, from reentry around a non-conductive bloc and by )triggering) by an e'ternal source. Reentry %eentry is often the cause of )tachy-arrhythmias). >hen there is ischemic, infarcted or necrotic conductive tissue around the bundles, with a difference in conduction speed around the defect there can be a reentry of the downward propagating depolariHation. >e see below the signal catching a section of the bundle ready to be repolariHed, but by this ectopic signal, not by the ne't signal coming from the &8 node above. The most common cause of pathologic tachycardias and arrhythmias results from reentry. This is due to a signal splitting around a defect and one side of that split being conducted significantly slower than the other

: /see below2. 3f the slow signal meet s the fast side ready to be depolariHed it can cause both normal and retrograde depolariHation. This can cause tachyarrhythmias due to the uncontrolled reentry.

Etiology of reentry

Sinu/ Ta2:y2ardia This rhythm originates in the non-pathologic state from an increase in demand for cardiac output, which is successfully met by the heart and whose rhythm originates in the &8 node. This is usually a remedy to a systemic process such as by hypovolemia, hypotension, hypo'ia, nervousness, medications and e'ercise. %emember that if the rate is high enough, the !-wave can be obscured in the &T-segment, but is still present= this is an artifact of the EKG machine, and if you set the scanning rate higher, you can reduce this problem. Supra%entri2ular Ta2:y2ardia/ !aro'ysmal 8trial Tachycardia /!8T2 This arrhythmia is seen with reentry in the atria. There is a circular conductive pathway in the atria, causing reentry to give a rapid tachycardia. There is a single ectopic pacema er, which can even be the 8; node itself. Lne feature often seen with this tachycardia will be inverted !-waves, due to the source being lower down in the atria. 8 diagnostic procedure that can be performed to separate this from sinus tachycardia is to do vagal maneuvers, and if the rhythm slows and then resumes after cessation of the maneuvers, sinus rhythm is present. 3f the rhythm terminates abruptly or thereAs no change, then itAs !8T.

!aro'ysmal 8trial Tachycardia

1ultifocal 8trial Tachycardia /18T2 This arrhythmia is seen with an ectopic pacema er somewhere in the atria. The abnormal pacema er cell, has stopped responding to the overdrive pacing from the sinus node. This causes there to be 2 or more asynchronous pacema ers for the heart. The hallmar of this form of &;T is the 2 or more !-wave morphologies you see= one !-wave from each pacema er. &urprisingly this rhythm can often be bro en by e'ercise or sinus-tachycardia= the reason for this, is that although the end result of 18T is tachycardia, each of the pacema ers is not tachycardia, it is the sum of their rates that produces the tachycardia. 3n e'ercise or other e'citatory states, the sinus node will overdrive pace the ectopic cells.

1ultifocal 8trial Tachycardia - %edMsinus node, 0lueMectopic

1+ 8trial (lutter The atria can also produce a flutter pattern, which is characteriHed by multiple sawtooth edged p-waves before each $%&, called <lutter;&a%e/. 3n atrial flutter, there are many ectopic pacema ers, in a more e'treme form of 18T. The atria are not actually contracting multiple times per $%& in this rhythm, but rather the multiple foci are summing on the EKG to a regular constructive-interference pattern. This rhythm is unstable, and will normally progress to atrial <ibrillation@

8trial (lutter

8trial (ibrillation The atria can also fibrillate, which is characteriHed by the complete absence of p-waves before each $%&. The other hallmar , is that he rhythm is Are1ularly irre1ularA. This means that there is no discernable pattern in the rate of ventricular beats. 8lso remember that the rate of conduction, is limited only by the 8; node= in conditions of rapid conduction, such as >olfe-!ar inson->hite />!>2 syndrome, where the conduction bypasses the node, the rate can approach 2++-*++bpmD 3n atrial fibrillation, there are a very large number of ectopic pacema ers and some reentry leading to random, ineffective "uivering of the atria. This is a serious rhythm, although fairly stable, and leads to an appro'imate 1+N drop in cardiac output, and has been lin ed to increased stro es due to the stasis of the blood in the atria.

8trial (ibrillation

8entri2ular Ta2:y2ardia >hen the rhythm originates in the ventricles, the intrinsic rate or automaticity is below .+ bpm. This can be seen in idioventricular rhythms when the &8 or 8; node are not the functioning pacema er of the heart. 4owever, when there is ischemic, infarcted or necrotic conductive tissue around the bundles, there can be a reentry of the downward propagating depolariHation, that causes the signal to repeat itself. This causes the very fast rate, as seen in ;entricular Tachycardia /often called ;-tach2= this can be a life threatening condition. The hallmar of ventricular rhythms is the &ide >RS 2o pleB. 0elow we see an e'ample of ;Tach, with a ventricular rate of 1,+bpm.

;entricular Tachycardia

'i1itali/ ToBi2ity
'i1itali/ is a very old cardiac drug derived from the FoB1lo%e plant, used in slowing conduction through the 8; node, usually in controlling the ventricular rate of atrial fibrillation. 3t is usually given in cases of atrial <ibrillation. Lverdoses of digitalis /either in the form of 'i1oBin or 'i1itoBin2 can have effects ranging from mild 1 E 8; bloc to ?unctional rhythms through fatal arrhythmias. The primary mechanism of action of digitalis is to suppress the 9a-K-8T!ase pump= this causes the membrane potential to be more positive, allowing for easier reaching of threshold, leading to action potentials. This creates a situation where it is easy to get spontaneous action potentials, leading to arrhythmias.

11 The most noticeable change to the EKG is the A/&oopin1A ST;/e1 ent depre//ion. 5ou also may see e'tended !% intervals or 1E bloc , although this alone is indistinguishable from primary 1E 8; 0loc . This will also be e'acerbated by hyponatremia or hyper alemia due to the failure of the 8T!ase pump to reestablish a membrane potential. 0elow we see an e'ample of the swooping &T-segment.

@igitalis To'icity

Hyper7ale ia
Cota//iu /K2 is one of the 2 ions that ma e up the bul of the ion-based membrane potential of cardiac cells /both myocytes and conduction cells2. 8n imbalance of potassium can create a life threatening situation which must be corrected immediately. The most prominent feature of an EKG of a hyper alemic patient is the pea ed-T wave. The other feature of the hyper alemic EKG is a stretching of entire waveform.

!ea ed-T >aves consistent with 4yper alemia

12

Credits

Aut:or/
Henry Feld an
4enry (eldman is a 1edical &tudent in the Blass of 2++1 at the 95F &chool of 1edicine. 4e is also a 1assachusetts licensed E1T, a 9ationally registered E1T as well as being 8B#& certified. 4e is the webmaster for the 95F &chool of 1edicine E% club >eb &ite. 4e also produced all the artwor in this publication. 4e is also an 848 B!% instructor. 4e can be reached at his mailto6feldmh+1Opopmail.med.nyu.edu

Mariano Rey! M'

1ariano %ey, Blass of 1:-. at the 95F &chool of 1edicine is the @irector of the 0ellevue Bardiac Blinic, Bo-director of the 95F Bardiac %ehabilitation and !revention Benter, co-director of the first-year medical physiology course, and is a faculty member of the 95F &chool of 1edicine. 4e can be reached at his mailto6reym+1Omcdad.med.nyu.edu

Ot:er Contributor/
'aniel Fi/:er! M'
@aniel (isher, is a clinical instructor in the @epartment of 1edicine, division of Bardiology. 4e is also the associate director of the 0ellevue &tress #aboratory. 4e is also the @irector of 3n-patient &ervices at the 95F Bardiac %ehabilitation and !revention Benter. 4e acted both as an editor and sounding board for parts of this publication. 4e can be reached at his mailto6fished+1Omcdad.med.nyu.edu

To download an 8crobat !@( format /better for printing, also with a Table of Bontents2 clic here. This page will help you learn to interpret 12-lead EKG patterns. This is not a comprehensive guide to EKG interpretation, and for further reading, the Dubin te'tboo is the introductory boo of choice. This te't was developed for use by 95F &chool of 1edicine students, but may be used by any medical teaching institution, without charge, as long as the document is not modified, distributed in its entirety and not used for profit, and may not be sold.

1*
Errors may be present in this document, and clinical use is at the ris of the user. Fsers should use their own clinical ?udgement in treating patients.