1. Standardiz ation. Make sure the standardization mark o n the EKG paper is 10 mm high so that 10 mm = 1 mV. Also make sure that the paper speed is correct.
2. Heart rate. Determine t he heart rate by the quick three-step m ethod described in Chapter 3.
3. Intervals. Measure the length of the PR and QT intervals and t he width ofs the QRS complexes.
4. QRS axis. Is t he axis no rmal, or is there axis deviation?
Diagnoses
5. Rhythm. Always ask The Four Questions:
Are there normal P waves present?
Are the QRS complexes wide o r narrow?
What is the relatio nship between the P waves and Q RS co mplexes?
Is the rhythm regular or irregular?
6. AV block. Apply the criteria in Chapter 4 .
7. Bundle branch block o r hemiblo ck. Apply the crit eria in Chapter 4 . 8. Preexcitation. Apply t he criteria in Chapt er 5 .
(Note that steps 6 thro ugh 8 all involve looking for disturbances of
P.277 conduction.)
9. Enlargement and hypertro phy. Apply the criteria fo r both atrial enlargement and ventricular hypertro phy.
10. Coro nary artery disease. L ook for Q waves and ST segment and T wave changes. Remember that not all such changes reflect coronary artery disease; know your differential diagnoses.
11. Utter confusion. Is there anything on the EKG you don' t underst and?
Never hesitate to ask for assistance.
The follo wing pages are memory joggers yo u can hang onto . Cut them out and stick them in that little black boo k of medical pearls t hat yo u no doubt carry around with you. Cut t hem out anyway, even if you don't carry a lit tle black book; t he exercise will do yo u go od after sitting and staring bleary-eyed at this book fo r so long.
The final chapter contains some sample EKGs for you to test yo urself with.
Some are easy; some are not. But here is one int erest ing fact: all of these patients were seen by one physician in a single day! T his sho uld give you an idea of how com mon EKG abnorm alities can be and how impo rtant it is to be able to read thedarn things.
And if you are still t hinking, “Is this really all there is to it? ”, the
answer—reminding you that informatio n only becomes knowledge with wisdom and experience—is, “Yes!”
P.278
P.279 Review Charts
The 12 Leads
The heart is compo sed of pacemaker cells, electrical conducting cells, and myo cardial cells. P acemaker cells depolariz e spo ntaneously and initiate each wave of depo larization. The SA no de is usually thedominant pacem aker.
Electrical conducting cells carry current rapidly and efficiently t o distant
regio ns o f the heart. Myo cardial cells co nstitute the bulk of the heart. When a wave of depo larization reaches a myo cardial cell, calcium is released within t he cell (excitation–co ntraction coupling), causing itto contract.
The P wave represents atrial depo larization. It is small and usually positive in the left lat eral and inferior leads. It is often biphasic in leads III and V1. Typically, it is m ost positive in lead II and most negative in lead AVR.
P.280
P.281 The QRS co mplex represents ventricular depo larization. It is usually
predo minantly positive in most lat eral and inferior leads. Acro ss the
precordium, the R waves increase in size, progressing fro m V1 to V5. A small initial Q wave, representing septal depolariz ation, can often be seen in the left lateral and inferior leads.
The T wave represents ventricular repolarization. It is the most variable waveform, but it is usually positive in leads with tall R waves.
The PR interval represents the time from the start of atrial depolarization to the start of ventricular depolarizat ion.
The PR segment is the time from the end o f at rial depolarizatio n t othe start of ventricular depolarizat ion.
The QRS interval represents the duration of the QRS com plex.
The ST segm ent represents the time from the end of ventricular depolariz ation to the start o f ventricular repolariz ation.
The QT interval represents the time from the start o f ventricular depolarization to the end of ventricular repolariz ation.
Calculating the Axis
Lead I Lead AVF
Normal axis + +
Left axis deviatio n + –
Right axis deviat ion – +
Extreme right axis deviation – – Atrial Enlargement
Loo k at the P wave in leads II and V1.
Right atrial enlargement is characterized by the following:
Increased amplitude of the first portion of the P wave 1.
No change in the duration of the P wave 2.
Po ssible right axis deviation of the P wave.
3.
Left atrial enlargement is characterized by the following:
Occasionally, increased amplitude of the terminal com ponent of theP wave 1.
More co nsistently, increased P wave duratio n 2.
No significant axis deviation.
3.
Ventricular Hypertrophy
Loo k at the QRS complexes in all leads.
Right vent ricular hypertrophy is characterized by the following:
P.282 Right axis deviatio n o f greater than 1 00°
1.
Ratio of R wave amplitude to S wave amplitude greater t han 1 in V1 and less than 1 in V6.
2.
Left ventricular hypertro phy is characterized by many criteria. The more that are present, the greater the likelihood t hat left ventricular hypertrophy is present.
Preco rdial criteria include the follo wing:
The R wave amplitude in V5 or V6 plus the S wave am plitude in V1 orV2
exceeds 35 mm . 1.
The R wave amplitude in V5 exceeds 2 6 mm.
2.
The R wave amplitude in V6 exceeds 1 8 mm.
3.
The R wave amplitude in V6 exceeds t he R wave am plitude in V5. 4.
Lim b lead criteria include the fo llowing:
The R wave amplitude in AVL exceeds 13 mm.
1.
The R wave amplitude in AVF exceeds 2 1 mm.
2.
The R wave amplitude in I exceeds 14 mm.
3.
The R wave amplitude in I plus the S wave amplitude in III exceeds 25 mm.
4.
The presence of repolarization abno rmalities (asym metric ST segment
depressio n and T wave inversion) indicates clinically significant hypert rophy, is mo st o ften seen in tho se leads with tall R waves, and may herald vent ricular dilatation and failure.
The four basic types of arrhythmias are:
Arrhythmias of sinus origin 1.
Ectopic rhythm s 2.
Co nduction blocks 3.
Preexcitation syndromes.
4.
Whenever you are interpreting t he heart' s rhythm , ask T he Fo ur Questions:
Are normal P waves present?
1.
Are the QRS complexes narro w (less than 0 .12 seconds in duratio n) or wide (greater than 0 .12 seconds)?
2.
What is the relationship between the P waves and the QRS complexes?
3.
Is the rhythm regular or irregular?
4.
The answers for normal sinus rhythm are:
Yes, P waves are present.
1.
The QRS complexes are narro w.
2.
P.283
P.284 There is one P wave for every QR S co mplex.
3.
The rhythm is regular.
4.
Characteristics EKG
PSVT Regular P waves are retrograde if visible
Rate: 150– 250 bpm
Carotid
massage: slows or terminates
Flutter Regular, saw-toothed 2:1, 3:1 , 4:1, etc., block Atrial rate:
250–35 0 bpm Vent ricular rate:
one half, one third, one fourth, etc., of the atrial rate Carotid
massage:
increases block
Fibrillation Irregular Undulating baseline Atrial rate:
350–50 0 bpm Vent ricular rate:
variable Carotid
massage: may slow ventricular rate
MAT Irregular
At least three different P wave morphologies Rate: 100– 200 bpm; sometimes less than 1 00 bpm
Carotid
massage: no
P.285 effect
PAT Regular
Rate: 100– 200 bpm
Characteristic warm-up period in the automatic form
Carotid
massage: no effect, or only mild slo wing
Ventricular Arrhythmias
Rules of Aberrancy
VT PSVT
Clinical Clues
Carotid m assage N o response May terminate
Cannon A waves May be present Not seen
EKG Clues
AV dissociatio n May be seen Not seen
Regularity Slightly irregular Very regular
P.286
P.287
Fusion beats May be seen Not seen
Initial Q RS deflection
May differ fro m normal QRS co mplex
Same as normal QR S complex
AV Blocks
AV block is diagnosed by examining the relationship of the P waves to the QR S complexes.
First degree: The PR interval is greater than 0.2 seconds; all beats are conducted through to the ventricles.
1.
Second degree: Only som e beats are co nduct ed through to the ventricles.
Mobitz type I (Wenckebach): Pro gressive prolongat ion of the PR interval until a QRS is dropped
a.
Mobitz type II: All-or-nothing co nduction, in which QRS com plexes are dropped without PR int erval prolo ngation
b.
2.
Third degree: No beats are conducted thro ugh to the vent ricles. There is complete heart block with AV dissociation, in which the atria and
ventricles are driven by independent pacemakers.
3.
Bundle Branch Blocks
Bundle branch block is diagnosed by loo king at the width and configuratio n of the QRS complexes.
Criteria for Right Bundle Branch Block
QRS com plex widened to greater than 0.12 seconds 1.
RSR' in leads V1 and V2 (rabbit ears) with ST segm ent depression and T 2.
P.288 wave inversio n
Reciprocal changes in leads V5, V6, I, and AVL.
3.
Criteria for Left Bundle Branch Block
QRS com plex widened to greater than 0.12 seconds 1.
Broad o r no tched R wave with prolo nged upst roke in leads V5, V6, I, and AVL with ST segment depressio n and T wave inversion
2.
Reciprocal changes in V1 and V2 3.
Left axis deviation may be present.
4.
Hemiblocks
Hemiblock is diagnosed by looking for left or right axis deviation.
Left Anterior Hemiblock
No rmal QRS duratio n and no ST segment o r T wave changes 1.
Left axis deviation greater than –30°
2.
No o ther cause o f left axis deviatio n is present.
3.
Left Posterior Hemiblock
No rmal QRS duratio n and no ST segment o r T wave changes 1.
Right axis deviatio n 2.
No o ther cause o f right axis deviatio n is present . 3.
Bifascicular Block
The features of right bundle branch blo ck co mbined with left anterior hemiblock are as follo ws:
Right Bundle Branch Block
QRS wider t han 0.12 seconds RSR' in V1 and V2.
Left Anterior Hemiblock
Left axis deviation.
The features of right bundle branch blo ck co mbined with left po sterior hemiblock are as follo ws:
Right Bundle Branch Block
RS wider than 0.12 seconds RSR' in V1 and V2.
Left Posterior Hemiblock
Right axis deviatio n.
P.289
P.290 Preexcitation
Criteria for WPW Syndrome
PR interval less than 0.12 seconds 1.
Wide QR S co mplexes 2.
Delta wave seen in so me leads.
3.
Criteria for LGL Syndrome
PR interval less than 0.12 seconds 1.
No rmal QRS width 2.
No delta wave.
3.
Arrhythmias com monly seen include the following:
Paro xysmal supraventricular tachycardia—narro w QRS complexes are more comm on than wide ones.
1.
Atrial fibrillation—can be very rapid and can lead to ventricular fibrillation.
2.
Myocardial Infarction
The diagno sis of a myocardial infarct ion is made by histo ry, physical
examinat ion, serial cardiac enz yme determinatio ns, and serial EKGs. During an acute infarctio n, the EK G evolves through three stages:
The T wave peaks (A), then inverts (B).
1.
The ST segment elevates (C).
2.
Q waves appear (D).
3.
Criteria for Significant Q Waves
The Q wave must be greater than 0.04 seco nds in durat ion.
1.
The depth of the Q wave must be at least one third the height of the R wave in the same QRS complex.
2.
Criteria for Non–Q Wave Infarctions
T wave inversio n.
1.
P.291
P.292
P.293 ST segment depressio n persisting for more than 48 ho urs in the
appro priate setting.
2.
Localizing the Infarct
Inferio r infarction: leads II, III, and AVF
Often caused by occlusion o f the right co ronary artery or its descending branch
Reciprocal changes in anterior and left lateral leads.
Lateral infarct ion: leads I, AVL, V5, and V6
Often caused by occlusion o f the left circum flex artery Reciprocal changes in inferior leads.
Anterio r infarct ion: any of the precordial leads (V1 thro ugh V6)
Often caused by occlusion o f the left anterior descending artery Reciprocal changes in inferior leads.
Po sterior infarctio n: reciprocal changes in lead V1 (ST-segment depressio n, tall R wave)
Often caused by occlusion o f the right co ronary artery.
The ST Segment
ST segment elevation may be seen:
With an evolving infarction 1.
In Prinzmetal's angina.
2.
ST segment depression may be seen:
With typical exertional angina 1.
In a non–Q wave infarction.
2.
ST depressio n is also one indicato r of a positive stress test.
Miscellaneous EKG Changes Electrolyte Disturbances
Hyperkalemia: Evolution of peaked T waves, PR prolongation and P wave flattening, and QRS widening. Ultimately, the Q RS co mplexes and T waves merge to fo rm a sine wave, and ventricular fibrillatio n m ay develop.
Hypo kalemia: ST depression, T wave flattening, U waves Hypo calcemia: Pro longed QT interval
Hypercalcem ia: Shortened QT interval.
P.294 Hypothermia
Osborne waves, pro longed intervals, sinus bradycardia, slow atrial fibrillatio n; beware of muscle tremor artifact.
Drugs
Digitalis: Therapeutic levels associated with ST segment and T wave changes in leads with tall R waves; toxic levels asso ciated with tachyarrhythmias and conductio n blocks; PAT with block is most characteristic.
Sotalol, quinidine, procainam ide, amio darone, tricyclic antidepressants, erythrom ycin, the quinolo nes, t he pheno thiazines, vario us antifungal medications, some antihistamines: P rolonged QT interval, U waves.
Other Cardiac Disorders
Pericarditis: Diffuse ST segment and T wave changes. A large effusion can cause low voltage and electrical alternans.
HOCM: Vent ricular hypertrophy, left axis deviation, septal Q waves Myocarditis: Conduction blocks.
Pulmonary Disorders
COP D: Low voltage, right axis deviation, poor R wave pro gression. Chronic cor pulm onale can produce P pulmo nale and right ventricular hypertro phy with repo larization abnormalities.
Acute pulmo nary em bolism: R ight ventricular hypertrophy with st rain, right bundle branch block, S1Q3. Sinus tachycardia and atrial fibrillation are the most com mon arrhythmias.
CNS Disease
Diffuse T wave inversio n, with T waves typically wide and deep; U waves.
The Athlete's Heart
Sinus bradycardia, no nspecific ST segment and T wave changes, left and right ventricular hypertrophy, incom plete right bundle branch blo ck, first-degree o r Wenckebach AV blo ck, occasional supraventricular arrhythmia.
P.296 Authors: Thaler, Malcolm S.
Title: Only EK G Book You'll Ever Need, The , 5th Edition Co pyright ©200 7 Lippinco tt Williams & Wilkins
> T a b l e o f C o nt e nt s > 9 . - H o w D o Y o u G e t t o C a r ne g i e H a l l ?
9.
How Do You Get to Carnegie Hall?1
The follo wing EKGs will allow yo u t o try out your new skills. U se the 11 -Step Method; do n't overlo ok anything; take your time. Ready? Here we go:
Sinus tachycardia. N ote also the presence of left axis deviation.
P.297 The rhythm is sinus tachycardia. D eep anterior Q waves and lateral Q
waves indicate an antero lateral myo cardial infarctio n.
P.298 The QR S co mplexes are wide and disto rted. In leads V5 and V6, the Q RS
co mplexes are notched, and there is ST segment depression and T wave inversion. This patient has left bundle branch block.
P.299 The bro ad, abnormal QR S co mplexes may imm ediately attract yo ur
att ent ion, but notice the pacer spikes befo re each one. T he spikes are preceded by a P wave (look at leads II, III, aVF, V1, and V2). This pacem aker fires whenever it senses a P wave, ensuring ventricular co nt ract ion.
P.300 N ote the deep Q waves in leads III and aVF. This tracing shows an inferio r
infarct.
P.301 The salient features here are the short PR interval, the broadened QR S
co mplex, and the telltale delta waves (best seen in leads aVL and aVF) of Wo lff-Parkinson-White syndro me.
P.302 The QR S co mplexes are greatly widened, with beautiful rabbit ears in lead
V1. This patient has right bundle branch block.
The rate is very fast and regular, and the QRS com plexes are narrow.
R etrograde P waves can be seen in lead III. This patient has a paroxysmal supraventricular tachycardia.
P.303 The rhythm is irregular, and the QRS complexes are narrow. This patient is
in at rial fibrillatio n.
Are you confused by what appears to be extrem e right axis deviatio n?
Actually, in this instance, the EKG electro des were accidentally
reversed— the right arm and left arm electro des were placed on the wrong arm s. When yo u see a tall R wave in lead AVR and a deep S wave in lead I, check your electro des.
Everywhere you lo ok you see dramatic ST segment elevat ion. This EKG shows an evolving infarct affecting the entire heart!
P.304
P.305 Yo u are staring at the classic saw-toothed pattern o f atrial flutter.
Left ventricular hypertrophy by all crit eria.
Wo lff-Parkinson-White syndro me.
Extrem e bradycardia resulting from hypo xemia in a patient with sleep apnea.
The initial rhythm is sinus, but not e t he disappearance of the P waves in the second half o f the strip. This second rhythm is an accelerated
junctio nal rhythm.
Ventricular tachycardia.