Podrid’s Real-World ECGs : A Master’s Approach to the Art and Practice of Clinical ECG Interpretation - Volume 3 - Conduction Abnormalities PDF

Volume 3, Conduction Abnormalities, explores the essentials of AV nodal and intraventricular conduction abnormalities seen in everyday clinical practice: AV conduction abnormalities, including first-, second-, and third-degree AV block and enhanced AV conduction Intraventricular conduction abnormalities, including intraventricular conduction delay, fascicular block, and bundle branch blocks. There are 101 cases included in Volume 3.

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Podrtd's Real-World ECGs A Master's Approach to the Art and Practice of Clinical ECG Interpretation

Volume3

Podrid's Real-World ECGs A Master's Approach to the Art and Practice of Clinical ECG Interpretation

Volume3 Philip Podrld, MD

Rahul Kakkar, MD

Professor of Medicine Professor of Pharmacology and Experimental Therapeutics Boston University School of Medicine

Cardiology Fellow Massachusetts General Hospital Harvard Medical School Boston, Massachusetts

Lecturer in Medicine Harvard Medical School Boston, Massachusetts Attending Physician West Roxbury VA Hospital West Roxbury, Massachusetts

Peter A. Noseworthy, MD Cardiology Fellow Massachusetts General Hospital Harvard Medical School Boston, Massachusetts

Rajeev Malhotra, MD, MS Instructor in Medicine Cardiology Division Massachusetts General Hospital Harvard Medical School Boston, Massachusetts

IJ cardiotext. PUBLISHING

Minneapolis, Minnesota

C 2013 Philip Podxid, Rajeev Malhotra, Rahul Kakkar, and Pete:r A. Nooeworthy

Due to ongoing research, discoveries, modific:ationa to medicines, equipment and device•, and change• in government regulations, the: information contained in thi& book

Cardiote> Rwa\'tl In ltt.dsll1nd1VF (Ito. rS mOiphclogy) ·~left «XXI~ -30" and -90')

Introduction: Conduction Abnormalities

~--------------------------------------------------------------

Conduction Abnormality

lnf8rdfon Qrmorphology lnolal'lu an lnl'llrction pettetn -when present In leldsl~lll.~nd~VF. n!Prt!lents lrlerlotWIII myoardlll rnlircUon -when present In lelds 11nd ~VI. repraents lltet~l Wllll III)'OOII'd llllnl'vc:Uon

rS mOtpiiGiotrlncllclttll 1 CIOI1Ciuctlon lllnOtmalit)' -when pte.~ent In let.ds II, II~ and aVF, n!fi~IS left anteffat f&Kfallar bloclt -when prmnt In IMd I (llllld aVI.), retOI'eJCflts left posletfat fllllclcullr blOCk

inferior wall MI, which is not a conduction problem. Indeed, a left anterior fascicular block cannot be diagnosed in the presence of an inferior wall infam.ion pattern.

Left Posterior FasciCNlar Block With a le.ft posterior fascicular block, le.ft ventricular activation is via the left anterior fascicle and the direction of impulse transmission is inferiorly and to the right (PIGUBl!. 4 ). Hence a left postcr.ior fascicular block results in a right axis (between +.90" and +180"). There is a negative QRS complex in lead I and a positive QRS complex in leads n and aVP. The QRS complex has an rS morphology in lead LIn contrast, a lateral wall MI, which is not a conduction abnormality, will also be associated with a right axis {FIGURE 3). However, in this situation the QRS complex has a Qr morphology as the infarction results in the initial activation going away from the lateral wall and hence from left to right. There are several other causes for a right axis in addition to a late.ral wall MI, and these must be considered before establishing the right axis as a left posterior fascicular block, which i$ a diagno$is of exclusion. Other cause$ for a right axis include: • !tight ventricular hypertrophy, which is diagnosed by the presence of a tall R wave in lead Vl and P pulmonale (right atrial hypertrophy or abnormality}

EIKtrical axis dlr«ted rlghlwlnl (rlghtaxlslnflontll pllne)

•Norm1l QRS ccrnplex dun~tlon (>; 0.10 sec) In lllllelldl • l\legll'-'eQRSc:omplelcl~lead I(S\IIIIIIIl> Rwwe; 1t. Rs complex) and positive QRS c:omplex 0111 RwavtJ In le.adsllandaVF

• R4ht-left arm lc:ad switch, whkh is associated with negative P and T wana in leads I and aVL and positive P and T waves and a positive QRS complex: in lead aVR

•Aightull~+Wind+110')

Flgunt 4. Lett poatMior faac:leuiU'IIIIIeeiL

7

Podrld's Real-World ECGs

• Dextrocardia, in which there is a pattern that resembles right-left arm lead switch (it:, an inverted P wave in leads I and aVL, a positive QRS complex, and positive P and T waves in lead aVR), as well as reverse R-wave progression across the precordium • Wolff-Parkinson-White syndrome, with negative delta waves in leads I and aVL that are indicative of a left lateral pathway • A biventricular pacemaker, in which the initial waveform of the QRS complex in lead I is a Q wave or QS pattern. However, most often a biventricular pacemaker is associated with an indeterminate axis.

with a left anterior fascicular block or an inferior wall MI (which shifts the axis leftward). An indeterminate axis may appear to be present if an old lateral and inferior wall MI is evident. However, in this case there are Q waves in leads I, II, III, and aVF and hence the axis shih is the result of an infarction. The presence of a lateral wall MI (which has a right axis) with a left anterior fascicular block (which has a left axis) or an inferior wall MI (which has a left axis) with a left posterior fascicular block (which has a right axis) will also have an indeterminate axis. However, in this case the negative QRS complex in either lead I (with a lateral wall MI) or lead aVF (inferior

A broad and deep terminal S wave in a right bundle branch block (RBBB) may give the appearance of a right axis. However, in this

wall MI) is due to an infarction and not an axis shift. A right-left arm lead switch (which has a right axis) associated with either an inferior wall MI or a left anterior fascicular block (which has a left axis) will

case the terminal S wave represents delayed right ventricular activation and not a left ventricular force. In this situation the terminal S wave should be ignored and is not considered for axis determination.

have an indeterminate axis. Lastly, the presence of a deepS wave due to an RBBB may give the appearance of a negative QRS complex in lead I, and the presence of a left anterior fascicular block will give

Indetenninate Axis

the appearance of an indeterminate axis. In the presence of an RBBB the deep S wave in lead I is the result of terminal delay in right ven-

An indeterminate axis with a supraventricular complex is defined as an axis that is between -90" and +/-180". The QRS complex is negative in leads I and aVF. This may represent either a very extreme left axis or a very extreme right axis. In a human adult heart, it is unusual to see

tricular activation and is not considered as part of axis determination (which is the direction of impulse conduction within the left ventricle). An indeterminate axis associated with a wide QRS complex may be seen with any situation in which there is direct ventricular myocardial

an indeterminate axis with a supraventricular QRS complex. There is no type of conduction pattern through the normal His-Purkinje system

activation, including a ventricular complex, a paced complex (especially biventricular pacing), or a preexcitation pattern, specifically WolffParkinson-White.

that will result in an indeterminate axis. Thus an indeterminate axis is the result of the simultaneous presence of two different abnormalities. For example, an indeterminate axis may be seen when there is right ventricular hypertrophy (which shifts the axis rightward) associated

Intraventricular Conduction Delay An IVCD is a nonspecific QRS widening (QRS duration > 0.10 sec) without any specific bundle branch block pattern. Conduction is

8

Introduction: Conduction Abnormalities still via the entire His-Purkinjc system, but it is slower than normal, accounting for the QRS widening. When the QRS complex is longer

or left ventricle. As the activation of the ventricles is via the: normal His-Purkinje system, abnormalities of the right or left ventricular myo-

than 0.10 second but shorter than 0.12 second and bas an R888 pattern (ie, an RSR' complex in lead Vl), it is often called an incomplete

cardium can be diagnosed. This is in contrast to an LBBB or RBBB in which ventricular activation is not via the normal conduction system,

RBBB. When the QRS complex is longer than 0.10 second but shorter than 0.12 second with a left bundle branch block (LBBB) pattern, it

but rather is via an abnormal pathway with direct myocardial activation. Hence abnormalities of the ventricular myocardium served by the

is often called in incomplete LBBB. However, the term incomplete

particular bundle cannot be diagnosed.

bundle branch bled: is not accurate because conduction through the His-Purk.inje system and bundle is all or none and will not be incom-

A QRS complex duration exceeding 0.12 second is also termed an IVCD if there is no specific bundle branch block pattern present.

plete. Hence a more appropriate term is an IVCD to either the right

IVCDs with QRS complexes that are very wide (> 0.18 sec) without a bundle branch bloclt pattern may be seen with severe dilated ca.rdiomyopauhy or hypcrlcalemia. The only etiology for a QRS complex duration exceeding 0.24 second is hyperkalemia, which is a medical cmcrgcnc.y that requires immediate therapy. In the absence of hyperkalemia, a bundle branch block, a ventricular complex, or a severe cardiomyopathy is not a56oc:iated with a QRS complex that is this wide.

Bt11Ulle Bf'tltu:b Blocks There may be failure of impulse conduction (] and broadS wave in leads I and V5-V6 [+-]).The axis is normal, between o• and +90• (positive QRS

QT/QTc intervals are normal (520/435 msec and 480/400 msec when the prolonged QRS complex duration is considered). continue$

77

Podrld's Real-World ECGs

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EC& 13B Analyaia: Complete heart lllack wHh ventricular escape rhythm wltlla left llundle branch lllack marphalagy and Intermittent capture (AV conduction)

78

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Conduction Abnormalities: Core Case 13

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ _ _

In ECG 13B, there is a regular rhythm at a rate of 42 bpm. There are regular P waves(*) at an atrial rate of 98 bpm. Some of the P waves are not obvious as they are within the QRS complex. However, when seen, the P waves are regular with a stable rate. The P waves are positive in

bundle branch block pattern. Therefore, the QRS complexes in this ECG are ventricular (ie, there is a ventricular escape rhythm). The last QRS complex("') is different and has aPR interval of 0.32 second (-30"). Some authors consider an extreme left axis as >-45" or

LAFB in the absence of apparent organic heart disease and not associ-

>-60". A fascicular block results in an axis shift but does not cause any widening of the QRS complex. A widened QRS complex indicates the presence of an intraventricular conduction delay in addition to the fascicular block or might be an associated right bundle branch block.

ated with block in the other fascicles is usually benign and infrequently progresses to bifascicular disease or complete heart block. There is no reason for any additional workup or therapy. •

rence of a full left bundle branch block in the future.

141 tahir99-VRG & vip.persianss.ir

Notes

tahir99-VRG & vip.persianss.ir

A

72-year-old man 11 llrought to tile emergencr department after he suddenly loet coniCIOUineaa willie tettlng out crflled. The IJIICOpal epiiOde wu olllernd by hla wife, who called 811. The man atatea tllat tile episode waa preceded bJ a ftellno or nahtheadedneM and welkneM. He al1o reportl tllethe has had alldomlnal cramps associated with diarrhea, nauaea, vo111tlng, and anorexia for tile past 2 daya,

during which time he hal been unable to take In anrtlllnt orally. When emeroencr medical •ervlces arrived, he •a• awake but diaphoretic and nauaeated. In the emergency departmtnt ht relate& a hlatory IJf a prnloua myoeardlal Infarction (MI) but no other cardiac or medical problem•. Ill current medication• are aspirin, slmvastatln, low-dose llslnoprll, and low-dose metoprolol. The p11y11ea1 ua1111 unre11ark8llle;

hla blood prealurela11t/80 m11 Hg. Lalloratory date are unremar1cable, except ror a blood urea nltroten level IJf 46 mgldl and a creellnlne lt~el of 1.3 mgldL. An ECG 11 obtained.

What abnormality Is seen? Does the ECG suggest an etiology for the syncopal episode?

148 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

Vl

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EC6 27 Analysis: Normal sinus rllytllm, first-degree AV llleck (prolonged AV conduction), right llundle llranch lllock, left uls, aid lnferler Will Ml

144

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 27

There is a regular rhythm at a rate of 84 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.28 sec). The P waves are positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm with first-degree AV block (prolonged AV con-

disease. However, if trifascicular disease were present, the occurrence of syncope would suggest a more advanced conduction abnormality (ie, complete heart block with an escape ventricular rhythm). In this situation, further evaluation of the conduction system would be indi-

duction). The QRS complex duration is prolonged (0.14 sec), and it has a right bundle branch block (RBBB) morphology with an RSR' complex in lead Vl (-->) and a broad terminalS wave in leads I and

cated. However, the presence of first-degree AV block in association

V5-V6 (..---).The QT/QTc intervals are prolonged (420/500 msec) but are normal when the prolonged QRS complex duration is considered (360/430 msec). The axis is extremely leftward, between -30" and -90" (positive QRS complex in lead I and negative QRS complex in leads II and aVF). While the axis is consistent with a left anterior fascicular block (LAFB ), the QRS complex has a QS morphology in leads II and aVF U), which is indicative of an old inferior wall myocardial infarction (MI). In contrast, a left anterior fascicular block has an rS morphology in leads II and aVF. Hence the left axis is not the result of a conduction abnormality but rather is due to an infarction.

with bifascicular disease (ie, RBBB and LAFB, if present) does not necessarily imply trifascicular disease as the prolonged PR interval might reflect an AV nodal conduction abnormality or slowing of conduction in the remaining fascicle (ie, the left posterior fascicle). In this case, since the left axis is not the result of an LAFB, the only definite conduction abnormality of the His-Purkinje system is an RBBB, while the first-degree AV block might be AV nodal or involve the remaining fascicles. This makes syncope from complete heart block far less likely. Indeed, the history strongly suggests that the patient was dehydrated as a result of 2 days of diarrhea, vomiting, and decreased oral intake. Further support for a diagnosis of volume depletion is the elevated blood urea nitrogen level, which is out of proportion to the serum creatinine level. The syncopal episode following a change in position is consistent with hypotension or perhaps a vasovagal episode as the etiology for the syncope. •

The ECG suggests trifascicular conduction disease (ie, RBBB, left axis, and first-degree block). However, the left axis is due to an inferior wall MI and not a conduction abnormality; hence this is not trifascicular

145 tahir99-VRG & vip.persianss.ir

Notes

tahir99-VRG & vip.persianss.ir

A n aaymptGmatlc 58-yaar-old man praaanta for a routine checkup. His vital slg~ts, phyalcal exam, and generallabornry twaluatlolt are all normal. An EC& Is obtained.

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147 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

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EC& 28 Analyaia: Normal sinus rllytllm, lett posterior fascicular lllock

148

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 28

The rhythm is regular at a rate of 62 bpm. There is a P wave (*) before each QRS complex with a stable PR interval (0.16 sec). The P wave is positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The QRS complex is of normal duration (0.08 sec) and morphology. The QT/QTc intervals are normal (360/370 msec). The QRS complex is negative in lead I and positive in lead aVF. Hence the axis is rightward (between +90" and +180"). There are several etiologies for a right axis, including: • Lateral wall infarct pattern, that is, an initial Q wave (Qr or QS) in leads I and aVL • Right ventricular hypertrophy, which will be associated with a tall R wave in lead Vt and evidence of right atrial hypertrophy or abnormality (P pulmonale) • Right-left arm lead switch, which is associated with negative P and T waves in leads I and aVL and positive P and T waves and positive QRS complexes in lead aVR • Dextrocardia, in which there are inverted P and T waves in leads I and aVL and reverse R-wave progression across the precordium • Right bundle branch block with a deep and broad S wave

• Wolff-Parkinson-White (WPW) pattern, which will be associated with a short PR interval and widened QRS complex resulting from a delta wave • Biventricular pacemaker, which will have a QS or deep Q wave in lead I. Most often an indeterminate axis will be seen. With a pacemaker, pacemaker stimuli will be seen. • Left posterior fascicular block (LPFB ), with all left ventricular forces originating from the left anterior fascicle and directed down and to the right. This diagnosis is made when all other causes for a right axis have been excluded. In this tracing, the QRS complexes have an initial R wave in leads I and aVL (rS complex), and there is no evidence for right ventricular hypertrophy, arm lead switch, dextrocardia, lateral infarction, WPW pattern, right bundle branch block, or pacemaker. Hence the right axis is due to an LPFB. The left bundle divides into two major fascicles that innervate the left ventricle. The left anterior fascicle crosses the left ventricular outflow tract and terminates in the Purkinje system of the anterolateral wall of the left ventricle. The left posterior fascicle appears as an extension of the main bundle and fans out extensively posteriorly toward the

in lead I may be diagnosed as a right axis. In this situation the

papillary muscle and inferoposteriorly toward the free wall of the left

terminal S wave, which reflects delayed right ventricular activation, should be ignored as it is not reflective of left ventricular activation and hence not considered as part of axis determination.

ventricle. There is often a third, smaller fascicle that is a septal branch (median fascicle) that innervates the interventricular septum, which continues

149 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

Conduction Abnormalities: Core Case 28

-------------------------------------------

is the first part of the left ventricle to be activated (in a left-to-right direction). The leh posterior fascicle is exposed to lower pressures and less turbulence than the left anterior fascicle; it also has a dual blood supply. These characteristics probably explain why isolated LPFB is an

acute cor pulmonale and, perhaps most commonly, chronic degenerative and fibrotic processes of the conducting system. An LPFB does not cause widening of the QRS complex, only a shift in axis. Hence any QRS widening is due to an associated intraventricular conduction dday

uncommon finding. Isolated LPFB can, however, be seen in the setting

or a right bundle branch block.

of extensive arteriosclerotic cardiovascular disease, as an association with inferior wall myocardial infarction and extensive coronary disease with diffuse myocardial fibrosis. LPFB can also occur with cardiomyopathies, hypertension with hypertrophy, myocarditis, hyperkalemia,

Isolated LPFB does not require any additional evaluation or therapy. However, additional evaluation may be required if there is evidence of

150

trifascicular disease. •

tahir99-VRG & vip.persianss.ir

A

54-,ear-old man preaenta 1o hla pr111ar, doctor aa a new patsent. He hat never had anr 11eanlntful medlc11 care In the paat. He comea today with co11plalnt1 of 1hortneas of breath with ever,da, actstltlat1hat has progrea1ed to 1he point 1hat he cannot aacend a flight of atalrt or even e alight trtde Incline without taking frequent restsfo catch his breath. His review of SJStems II notable for a 40-pound unlntlntsonalwelght 1011 over the past Jeer. He haa no known p•t medical hlltory 1nd doll not take anr 11edlcatlona. Hie famll, and social hlltllrlee are ramarkable for 35-Jear emploJiftent aa a

coal miner. He amoktd cltarettaa regular!, for 20 years but quit 10 yeart ago. On 0111, he appeers emeclettcl. His ha1rt rate Is 80 bp11, his blood prassure Is 112180 m11 Hg, and hl1llps are faints, blue. Hla head, ear&, eps, noae, and throat exam 11 notable for tamporal wasting. 111 luntt are I!Jperlnflettd with poor elr movament. Hit Jugular venous pressure Is 10 em H20 wltll taller CV wavaa. His precordium demonatratua right ventricular IIH. 111 point of maxlmallmpul" 11 nondlsplaced. 111 rhJ1hm 11 regular, with a normal S1 1nd prominent P2. Ar•plroph•lc holos,•tollc mur11ur Ia noted at the right lower atlmal border.

His 1bdo11ln11, extre11lty, end neurologic uams are normal. Arterial blood g1111 conftrm hypoxtmla and hypercapnia. An ECS II o~lned aa part of hla evaluetlon.

What abnormalities are noted? To what cardiopulmonary process do these abnormalities point, as suggested by his exam and hiSIOI'f?

151 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

EC6 29 Analyaia: lormal sinus rhythm, lntrnentrlcular conductlen delay, right axis, right atrial hypenrephy {abnormality), P pulmenale, right ventricular hypertrephy {RVH) wnh ST-T wave changes, premature atrial cemplex,left ventricular h,penrephy {LVH) with ST-T wawa changes, biwantricular h,penrephy

152

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 29

The rhythm is regular at a rate of 90 bpm. There is a P wave (*) before

abnormalities in leads V4-V6 (&)are likely the result ofLVH. The lOth

each QRS complex with a stable PR interval (0.20 sec). The P waves are positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The P waves are very tall in leads II and aVF and also positive

QRS complex (f) is early, is preceded by a premature P wave (+), and has the same QRS complex morphology as the sinus complexes. Hence it is a premature atrial complex.

and tall in leads Vl-V2; this is characteristic of right atrial hypertrophy or abnormality (P pulmonale). Given the height of the P waves in leads Vl-V2, the term "Himalayan P waves~ has been used. The QRS duration is slightly increased (0.12 sec), and there is an intraventricular conduction delay. The axis is rightward, between +90" and +180" (negative QRS complex in lead I and positive QRS complex in lead aVF). The

This patient has signs, symptoms, and ECG evidence of RVH, the result of chronic obstructive lung disease from coal dust exposure as well as cigarette smoking. There is also evidence on the physical exam of tricuspid regurgitation (respirophasic holosystolic murmur and tall CV waves of the jugular pulsation). The patient should have an

QT/QTc intervals are prolonged (440/540 msec) even when the slightly prolonged QRS complex duration is considered (420/490 msec). There

echocardiogram to evaluate pulmonary artery and right-sided pressures as well as left ventricular function. Initial therapy for pulmonary arte-

is a tall R wave (+-) in lead Vl. When associated with a right axis and P pulmonale, the tall R wave in lead Vl is indicative of right ventricular hypertrophy (RVH). Hence the right axis is the result of RVH and is not due to a left posterior fascicular block.

rial hypertension as well as chronic obstructive lung disease consists of oxygen therapy. As there is no clinical evidence for fluid accumulation, diuretics are not needed. More advanced therapy includes treatment with prostanoids such as epoprostenol, endothelin receptor antagonists,

In addition, the S-wave depth in lead V2 is 26 mm [ [ ), and the R-wave amplitude in lead V4 is 22 mm [] ] (S-wave depth in lead V2 + R-wave

phosphodiesterase 5 inhibitors such as sildenafil, or certain calciumchannel blockers (eg, a dihydropyridine or diltiazem). Patients with

amplitude in lead V4 = 48 mm), meeting the voltage criteria for left ventricular hypertrophy (LVH; S-wave depth+ R-wave amplitude in any two precordial leads ~ 35 mm). Therefore, there is evidence

pulmonary hypertension who are selected for advanced therapy should undergo an invasive hemodynamic assessment prior to the initiation of advanced therapy. A vasoreactivity test with intravenous adenosine, intravenous epoprostenol, or inhaled nitric oxide is often performed

of biventricular hypertrophy. There are also ST-T wave abnormalities in leads Vl-V3 ("),likely the result of RVH, while the ST-T wave

previous hypertension, although there is no clear history for this. •

at the time of hemodynamic assessment. The LVH may be the result of

153 tahir99-VRG & vip.persianss.ir

Notes

tahir99-VRG & vip.persianss.ir

A 18-yaar-old diabetic w•an praaanta to her primary care pllplclan K as a •ew patient. Site states ~~tat •She had some ~teart 1reublt In tile peat" but Ia unaware of any apaclftc dlagnoala.lheltaa atopptd taking all mtdlcatlo~t~ that were previously prescribed. She deClares, •11o, I'm dOIItD flltll" to Ill IIUIItlona Olt I review of system&. Her VItal 111n1 and exam are unremarkable. Aa part of her naluatlon, an ECI Ia parfermad. I

What abnormalities are noted on the ECG, and to what pathology do they point?

V«

155 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

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ll EC6 30 Analysis: lormal sinus rhythm, first-degree AV lllock (prolonged AV conduction), right ax11, old lateral waiiiiiJocardlal Infarction (MI), old anterior wall Ml, left atrlalllypertrophy (allnermallty)

158

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 30

There is a regular rhythm at a rate of 86 bpm. There is a P wave (*) before each QRS complex with a stable PR interval of 0.22 second. The P wave is positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm with first-degree AV block (prolonged AV conduction).

Although the patient does not provide any history to suggest a prior MI or its timing, the presence of Q waves indicates that the infarction is chronic or old. Although she claims a history of some heart problem in the past, she provides no specifics about this. Silent infarc-

However, the P waves are broad in leads II and aVF ("), suggesting

tions are not uncommon, especially in the diabetic patient. Her therapy

left atrial hypertrophy or abnormality. The QRS complex duration is normal (0.10 sec). The axis is rightward, between +90" and +180" (neg-

should consist of aggressive risk factor modification, including aspirin; LDL-lowering therapy with statins; and good control of her diabetes.

ative QRS complex in lead I and positive QRS complex in lead aVF). However, the right axis is a result of a Q wave (). The initial 0.08 second of the QRS complex is normal and the increased QRS duration is a result of the R', which represents a delay in right ventricular activation, with the terminal forces being directed from left to right (toward lead V1). Leads I and V5-V6 have broadS waves(+-) that also represent the terminal forces being directed from left to right (away from these leads), a result of delayed right ventricular activation. This is a pattern that indicates the presence of a right bundle branch block (RBBB). There are T-wave changes(") in leads Vl-V2 that are due to the RBBB. Although the R' in lead Vl is very tall in amplitude, a diagnosis of right ventricular hypertrophy cannot be made on the ECG in the presence of an RBBB as right ventricular activation is abnormal, not occurring through the normal His-Purkinje system but rather directly through the right ventricular myocardium.

An RBBB is identified by the following characteristics: • The QRS complex duration is 0.12 second or longer due to delayed activation of the right ventricle. • Delayed right ventricular activation occurs directly through the right ventricular myocardium originating from the left bundle and left ventricle. Right ventricular activation, therefore, bypasses the normal His-Purkinje system. The terminal forces of the QRS complex are directed from left to right. Since conduction velocity is slow (due to direct myocardial conduction) the terminal forces are delayed, accounting for the widened QRS complex. Hence there is an RSR' complex in leads V1-V2 (due to delayed right ventricular forces directed toward the right-sided leads Vl-V2) and broadS waves in leads I and V5-V6 (due to delayed right ventricular forces directed away from the left). • Right ventricular repolarization is also abnormal, and secondary ST-T wave changes are often seen in leads V1-V3. • Since right ventricular activation is abnormal, right ventricular hypertrophy cannot be recognized. • Since left ventricular activation is normal, the initial portion of the QRS complex (first 0.08 sec) is normal. Abnormalities affecting the left ventricle can be recognized (eg, left ventricular hypertrophy, infarction, ischemia, pericarditis).

193 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

• An RBBB may also be associated with conduction abnormalities of the fascicles of the left bundle (ie, a left anterior or left posterior fascicular block). This is established by the presence of an extreme left or right axis in addition to the RBBB. The presence of an RBBB and fascicular block is termed bifascicular disease. • An RBBB may be intermittent or related to increased heart rate (rate-related RBBB). • A QRS complex duration of 0.10 to 0.12 second in conjunction with an RBBB-like morphology has been termed an incomplete RBBB. However, as conduction through the RBBB is all or none, it is more appropriate to term this an intraventricular conduction delay to the right ventricle.

Conduction Abnormalities: Core Case 38

There are multiple etiologies of isolated RBBB. Any entity that raises pulmonary pressures and induces geometric alteration of the right bundle may impair right bundle conduction. This is often in association with a rightward shift in the axis in the frontal plane. Cardiomyopathies, myocardial fibrosis from infarction, and myocarditis may also cause RBBB, generally with other ECG findings consistent with the underlying diagnosis. Idiopathic conduction system disease (Lev's or Lenegre's disease) may be isolated to the right bundle. In this case, chronic pulmonary emboli have likely raised pulmonary pressures to the point of right ventricular pressure overload (as evidenced by an elevated brain natriuretic peptide) but without physical findings of right ventricular hypertrophy or dilation (no parasternal lift on palpation, no murmur of tricuspid regurgitation). An echocardiogram would assist in evaluation of right ventricular morphology and pulmonary pressures. •

194

tahir99-VRG & vip.persianss.ir

A

48-ytar-old man with known outructlw aleep apnea preaenta til your clinic for routine evaluation. On review, the man ad111b that ht 11 noncompliant with hl1 contlnuou1 positiVI airway preuurt (CPAP} machine aa he 11 unable to eleep when wearing tile m111c. Due to eevert dJapnea, hla exerclae cepacltJ Ia llvtrtiJ diminished and he Is ll11lted to a11bullllna onlr within hll holle. He denlea orthopnea or anginal IJIIIptDma. Hla heart rate Ia 100 bpm, and hla blood prt~ture 1RI110 mm Hg. Hla reaplratory rate 11

t4'lfl on a11blent air. 111 bodJ m111 Index I• 42.

11 breatllllllln, and hll retina 01 1aturat1on 11

Hie lower e.xtramllea dl&plar mild pitting ede11a bilaterally. An ECS 11 obtained.

Cpnoala Ia abient. Hla lunaa are clear. Hla Jugular wnou1 preuure Is 14 em H10 wltll CV WIJ81. Ill cardlovaacular uam 11 notable for a precordial (rlaht vtntrlcular} lift, pulmonary artery tap, and a prominent P2 component of S2. A10ft holoayltollc murmur 11 noted at tile left lower stemal border. Carvallo'e 1lgn (resplratorr variation In tile lnten11ty and duration of the mur11ur} 11 noted. 111 abdo11an 11 protuberant wlllout aro11 hepatomegaly.

What abnormalities are shown? What Is the underlying cause of these abnormalities? What further diagnostic testing may be helpful?

185 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

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ECG 39 Analysis: Slnua tiCIIJclrdla, flrat-detre• AY block (pralonted AY conduction),

right bundle llrancb black, lift anterior fascicular lllock, blfasclcular lllock

118

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 39

There is a regular rhythm at a rate of 100 bpm. There is a P wave(*) before each QRS complex with a stable PR interval of 0.24 second. The P wave is positive in leads I, II, aVF, and V4-V6 (although it is of very low amplitude in these leads). Hence this is sinus tachycardia

branch block (LBBB) or RBBB with alternating left anterior or left posterior fascicular block. Other situations in which trifascicular block can be diagnosed include (1) bifascicular block (ie, LBBB or RBBB with either left anterior or left posterior fascicular block) associated with

with first-degree AV block (prolonged AV conduction). The complex

Mobitz type II block or (2) bifascicular block with development of

duration is prolonged at 0.16 second, and the morphology is that of a right bundle branch block (RBBB; tall, broad R wave in lead Vl [-+] and broadS waves in leads I and VS-V6 [] and broadS wave in leads I and V5-V6 [

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Podrld's Real-World ECGs

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Conduction Abnormalities: Core Case 42

The rhythm is regular at a rate of 86 bpm. There is a P wave(*) before each QRS complex with a stable PR interval (0.18 sec) ( n). The P wave is positive in leads I, II, aVF, and V4-V6. Hence there is a stable normal sinus rhythm. There are two different QRS morphologies, both

in the horizontal plane. This is determined by imagining the heart as viewed from under the diaphragm. In this situation, the right ventricle is in front and the left ventricle is to the left. With clockwise rotation the left ventricular forces are delayed and develop later, occurring in

of which are preceded by a P wave that has the same morphology; the PR interval of both QRS complexes is the same. The narrow QRS complex (+) has a normal duration (0.08 sec) and morphology. The axis is

anterior fascicular block. The QT/QTc intervals for the narrow QRS complexes are normal (320/380 msec). The QT/QTc intervals for the

extremely leftward, between -30" and -90" (positive QRS complex in lead I and negative QRS complex in leads II and aVF, with an rS complex). This is diagnostic for left anterior fascicular block.

QRS complexes with an RBBB are prolonged (380/455 msec) but are normal (320/380 msec) when correcting for the prolonged QRS complex duration.

Also noted are QRS complexes that are wide (.t) (0.14 sec) with a typical right bundle branch block (RBBB) morphology (RSR' mor-

Intermittent or rate-related RBBB is indicative of underlying conduction

the lateral precordial leads. Clockwise rotation can be seen with a left

phology in lead Vl 1~1 and broadS wave in leads I and V5-V6 [

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awallable tor r1¥11W. Hlalnltlel wllal 1lgn1 1r11table, with 1 blood pressure Of 130110 mm HI and 1 puiM of 72 bpm. PhyaiCII n~mlnatlon 11 unr~marllable, aHhough he II natad to 111 vary dlaplloretlc. IUtroaJycerlll IS llvtn for tile cllest dlacanrfart, pJOYidlnglncompleta r1U1f. Morpllhll II admlnlate.retl. A 12-lead ECI (471) II obtained.

What type of ••block• Is shown on the baseline ECG (47A)? What diagnosis can be made based on ECG 478? What therapy Is Indicated?

227 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECBs

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tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 47

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ _ _

ECG 47A shows a regular rhythm at a rate of 75 bpm. There is a P wave before each QRS complex(+), with a stable PR interval (0.18 sec). The P wave is positive in leads I, II, aVF, and V4-V6; therefore, this is a normal sinus rhythm. However, the P wave is broad and prominently

leftward, between -30" and -90". Although this axis is consistent

notched in leads II and V3-V6 and is negative in leads V1-V2. This is consistent with left atrial hypertrophy (or abnormality). The QRS complex duration is increased (0.14 sec) and it has a typical left bundle

cardium. There are ST-T wave changes in leads I, aVL, and V3-V6 (")

branch block (LBBB) morphology, with a broad R wave in leads I and V5-V6 ().The axis is extremely

duration is considered (380/425 msec).

with a left anterior fascicular block, this cannot be diagnosed in the presence of an LBBB as both fascicles (left anterior and left posterior) are blocked and not conducting an impulse to the ventricular myothat are secondary to the LBBB. The QT/QTc intervals are prolonged (420/470 msec) but are normal when the prolonged QRS complex continue$

229 tahir99-VRG & vip.persianss.ir

Podrld's Rail-World ECGs

EC6 478 AnaiJsls: Nermal sinus rhJtbm, left bundlt bnaclllllock, acut. Inferior wall and antln~lateralwtiiiiiJOCardllllllfarctlon

230

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 47

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ _ _

In ECG 47B the rhythm is regular at a rate of 72 bpm. There is a P wave before each QRS complex(+) with a stable PR interval (0.18 sec). The P wave is positive in leads I, II, aVF, and V4-V6; hence this is a normal sinus rhythm. The QRS complex duration is increased (0.14 sec), and it has an LBBB morphology, with a broad R wave in leads I (-+) and V6 and a deep QS complex in lead Vl (+-).However, there is now significant ST-segment elevation Win leads II, III, aVF, and V5-V6 that ranges from 2 to 5 mm (t) as well as ST-segment depression in leads I and aVL (j). These ST-segment depressions are more pronounced than those in the baseline ECG (ECG 47A) and are reciprocal changes seen with an inferior wall myocardial infarction (MI). In addition, the T waves in leads II, III, aVF, and V5-V6 are tall, domed, and symmetric. These changes are diagnostic for an acute inferior and anterolateral wall ST-segment elevation MI. In the presence of an LBBB, left ventricular abnormalities (eg, left ventricular hypertrophy, pericarditis, ischemia, chronic MI, and axis) cannot be established reliably since left ventricular activation is no longer through the normal His-Purkinje system but instead is by direct myocardial activation from the right bundle and right ventricular

myocardium. However, an acute ST-segment MI can be established based on the Sgarbossa criteria:

1. ST-segment elevation of~ 1 to 2 mm that is in the same direction (concordant) as the QRS complex in any lead. 2. ST-segment depression of~ 1 mm in any lead from Vl to V3 3. ST-segment elevation of~ 5 mm that is discordant with the QRS complex (ie, associated with a QS or rS complex) Although the Sgarbossa criteria have been reported in patients with an LBBB, the same criteria have been found to be useful with a paced QRS complex and are likely also useful whenever there is direct myocardial activation, which would also include a ventricular complex and a Wolff-Parkinson-White pattern. Even though this patient has an underlying LBBB, there are ECG changes that are diagnostic for an acute inferior wall ST-segment elevation MI, including the hyperacute T waves and the significant ST-segment elevation with reciprocal ST-segment depression. Important therapy would be prompt reperfusion either in the catheterization laboratory with percutaneous coronary intervention (stenting) or with a thrombolytic agent. •

231 tahir99-VRG & vip.persianss.ir

Notes

tahir99-VRG & vip.persianss.ir

U-year-old man wltllalllatory mild A llypertenslall, wall centralled an llydrecllloretlllazlde, praenta to tile emergency crt

department with signs and srmptoms crt acute llranchnls. He hu a preductlve couall and

law-grade temperatura and alu notH pleudtlc cllest pain. Achasti-ray and whttelllaed cell count are normal. An ECIIs olltalned, and tile •••rtency departMalll pllyslclan has sa•• conoarna about what It sllowa.

What Is the abnormality? Is It of any concern?

188 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

aVR

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ECG 48 AnaiJIII: lormal alnua rllythm, left ltrlalllypertropiiJ (abnennalltJ), nonspecific ST·T wave changll,lntraventrlcular cenductlon delaJ (Incomplete left bundlellrancllllleck)

284

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 48

There is a regular rhythm at a rate of 72 bpm. There is a P wave (*) before each QRS complex with a stable PR interval (0.20 sec). The P wave is positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The P waves are broad (0.16 sec) in leads II and aVF (+) and negative in lead Vl. These changes are consistent with left atrial hypertrophy (abnormality). The QRS complex duration is increased (0.11 sec) and there is a normal axis, between 0" and +90" (positive QRS complex in leads I and aVF). The QRS complex morphology is normal. There are nonspecific ST-T wave changes noted in leads I, II, aVL, and V5-V6 (").The QT/QTc intervals are slightly prolonged (430/470 msec) but are normal when the prolonged QRS complex duration is considered (400/440 msec). The major finding is the slightly prolonged QRS complex duration. Although it has a morphology resembling a left bundle branch block (LBBB; R wave in lead I and QS complex in lead Vl), it is not wide

widening of the QRS complex is actually an intraventricular conduction delay to the left ventricle. Although this seems like only semantics, it is clinically important. An LBBB (complete or incomplete) means that the activation of the left ventricle bypasses (or partially bypasses) the normal His-Purkinje system. Thus activation of the left ventricle is not via the normal Purkinje system but directly through the ventricular myocardium. Therefore, abnormalities that affect the left ventricle (eg, ischemia, myocardial infarction, pericarditis, left ventricular hypertrophy) cannot be diagnosed. The presence of an intraventricular conduction delay means that impulse conduction still occurs through the normal conduction system, but there is diffuse slowing of conduction through the Purkinje network and ventricular myocardium. As the normal conduction system is used, abnormalities that affect the left ventricle can still be diagnosed. As there is no major abnormality on the ECG, there is no reason for any

enough for a true or complete LBBB. Therefore, this has been termed

concern and no need for any additional evaluation aside from making

an incomplete LBBB. However, this is a misnomer since conduction through the bundles is all or none and not incomplete. The slight

certain that blood pressure is well controlled.

•

235 tahir99-VRG & vip.persianss.ir

Notes

tahir99-VRG & vip.persianss.ir

A

40-,e•-old woman who recaldiJ emigrated fro II Brall pr•ents to a primary care phJIIclan aa a new petlent. On review, 1he 1t1t11 thet 1he h11 become progr•slvely limited In her ac11wlty ner the put sneral mont111 bacauM of &hortn•• of bred. She denle& cheat dlacomfart, orthopnea, or chana• In weight. On eum, her heer1 rate 1112 bpm end lllood pre11ure II

11ti7G m11 Hg. Her head, eart, a,.a, noM, and tllroat eum 11 normal. Her Jugular vanoua pre11ure Ia 12 em H20 wltll Ku11meul'1 sign. Her luna• are cleer. Her precordium Is notablt for a diffuse point of maxl11al lllpulae. Hear1aound& are regular, and an 13 gallop 11 evident. Her abdo11an manlftltl a fluid waw. The remelnder IJf her 111m Ia normel. An lCG Ia obtllned.

What abnormalities are evident?

237 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

EC6 49 Analysis: lormal sinus rhythm, intraventricular conductien delay

288

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 49

There is a regular rhythm at a rate of 62 bpm. There is a P wave (*) before each QRS complex with a stable, short PR interval (0.12 sec). The QRS complex is wide (0.18 sec). Although the morphology looks like that of a left bundle branch block (broad R wave in leads I and

With a left bundle branch block, activation of the left ventricle is not via the normal His-Purkinje system but rather is by direct myocardial activation. In contrast, the presence of an intraventricular conduction delay indicates that left ventricular activation is occurring via the nor-

VS-V6 [+-] and deep S wave in lead Vl [-+]),there are small septal

Q waves(") in leads I, aVL, and VS-V6 and a prominent septal R wave

mal conduction system but is diffusely slowed. Since the impulse travels along the normal His-Purkinje system, abnormalities that affect the

in lead Vl (!). Septal Q waves cannot be present in a left bundle branch block, as septal activation is via the septal branch (median fascicle) from the left bundle. Hence the wide QRS complex is actually due to an intraventicular conduction delay. The QT/QTc intervals are pro-

left ventricle (eg, axis shift, acute and chronic myocardial infarction, ischemia, left ventricular hypertrophy, pericarditis) can be identified. Commonly a QRS complex that is this wide is the result of an underlying cardiomyopathy and is due to diffuse myocardial fibrosis and

longed (460/470 msec) but are normal when corrected for the wide QRS complex duration (360/370 msec).

therefore marked slowing of impulse conduction. There is in fact a correlation between the left ventricular ejection fraction and the QRS complex duration with an intraventricular conduction delay. •

239 tahir99-VRG & vip.persianss.ir

A &8-yaar-ald woman prasanta ta her phplclan with c•plalnts K of progrt881ve shert•ess Of breatlt. She II k•own to ltave nenlscllamlc dilated cardlamppatlly with a left ventricular a)actlan fractlen of 48~. llut she ltas never !tad heart flllure. PllySIOII exam demonatratea an S3, a mur.ur Of mitral reguranatlon, a•d blllaallar reles. Her heart rate 11128 llpm, end an ECI demonstrates alnua

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242

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 50

ECG SOA shows a regular rhythm at a rate of 46 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.32 sec). A second P wave W can be seen after each QRS complex. In some leads (V2-V3) the P wave is superimposed on the upstroke

prolonged (520/455 msec) but are normal when the prolonged QRS complex duration is considered (440/385 msec). Therefore, there is bifascicular disease (right bundle branch block and

of the T wave ("),causing a notching of this waveform. The PP interval is slightly irregular (U), and the average atrial rate is 92 bpm.

left anterior fascicular block) as well as first-degree AV block (prolonged AV conduction). Although this might be considered to represent tri-

It can be seen that the PP interval surrounding the QRS complex is

slightly shorter (0.60 sec) than the PP interval without a QRS complex (0.66 sec). This is termed ventriculophasic arrhythmia and is due to acute acceleration of sinus node activity with ventricular contraction.

fascicular disease, this diagnosis cannot be established by this EC G as the first-degree AV block may be the result of either AV nodal disease (which would not be trifascicular disease) or disease of the remaining fascicle (which would represent trifascicular disease). Even though there

This may be seen with either 2:1 AV block or complete (third-degree)

is also second-degree AV block present with a pattern of 2:1 conduc-

AV block. Proposed mechanisms include acceleration of sinus node automaticity due to augmentation of pulsatile blood flow through the sinus node artery, stretch of the right atrium resulting from ventricular contraction, or changes in autonomic tone due to changes in baroreceptor activity resulting from a stroke volume.

tion, this may be either Mobitz type I or Mobitz type II. If the 2:1 AV block is Mobitz type II, then trifascicular disease can be diagnosed. If the 2:1 AV block is Mobitz type I, which is an AV nodal abnormality, then this would be bifascicular disease as well as AV nodal disease. The etiology of the 2:1 AV block can only be established if there was

The P waves are positive in leads I, II, aVF, and V4-V6. Hence there is a normal sinus rhythm with first-degree AV block (prolonged AV conduc-

a change in the pattern of AV nodal conduction. Thus, if there were several sequential P waves that were conducted with a stable PR inter-

tion) and second-degree AV block with 2:1 conduction (2:1 AV block). The QRS complex duration is increased (0.16 sec), and it has a morphology of a typical right bundle branch block (RSR' complex in

val, then the diagnosis would be Mobitz type II. If the P waves were conducted with a progressive increase in the PR interval, the diagnosis would be Mobitz type I. If complete heart block were to develop, the etiology of the escape rhythm would also establish the etiology of the

lead Vl [-+]and a broad terminalS wave in leads I and V5-V6 [+-]). The axis is very leftward, between -30" and -90" (positive QRS com-

etiology would be Mobitz type I, while an escape ventricular rhythm

plex in lead I and negative QRS complex in leads II and aVF, with an rS morphology). As the QRS complex has an rS morphology, this is a left anterior fascicular block. The QT/QTc intervals are slightly

2:1 AV block. That is, if there was a junctional escape rhythm the would establish Mobitz type II as the etiology.

continues

243 tahir99-VRG & vip.persianss.ir

Podrld's Real-World ECGs

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244

tahir99-VRG & vip.persianss.ir

Conduction Abnormalities: Core Case 50

rate is faster than the ventricular rate, this is complete or third-degree

In ECG SOB, there is a regular rhythm at a rate of 42 bpm. The QRS complex duration, morphology, and axis are identical to what was seen in ECG SOA (ie, right bundle branch block and left anterior fascicular block). The QT/QTc intervals are the same. P waves are seen (+), and

AV block. The QRS complexes are identical to those seen in ECG SOA, so the escape rhythm is junctional. Therefore, the 2:1 AV block seen on ECG SOA is a result of Mobitz type I. The conduction abnormalities are

the PP interval is fairly constant ( U) with an average atrial rate of

not the result of trifascicular disease but rather are due to bifascicular

84 bpm. As with ECG SOA, ventriculophasic arrhythmia is present and the PP interval surrounding the QRS complex (0.70 sec) is slightly

disease with associated AV nodal abnormality. As the complete heart block is a result of failure of AV nodal conduction, a Jl-blocker should not be administered as this could exacerbate the presence of complete heart block and might depress an escape junctional focus, resulting in a slowing of the junctional rate. •

shorter than the PP interval without an intervening QRS complex (0.78 sec) ( U). However, the PR intervals are variable ( n), particularly evident at the end of the ECG, indicating AV dissociation. As the atrial

245 tahir99-VRG & vip.persianss.ir

st-yeer-old men with e family hlatory .r audden death a•d dilated e~rdloMJtpathy presents to tile emergency department following 2 dey~ Of enreMe fatigue and llglltheadedness. On Initial

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What abnormalities are shown? What is the management?

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248

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Conduction Abnormalities: Cora Case 51

ECG SlA shows regular RR intervals at a rate of 30 bpm. There are P waves(*) seen, and they have a stable PP interval ( U) at a rate of 90 bpm. Some of the P waves are not apparent (+) as they are either on T waves or superimposed on the QRS complexes. However, the

a pattern of right bundle branch block (RBBB; RSR' morphology in lead Vl []).The axis is extremely leftward, between -30• and -90• (positive QRS complex in lead I and negative QRS complex in leads II and aVF, with an rS morphology),

PP intervals of the obvious P waves are regular ( U). The P waves are

indicating a left anterior fascicular block (LAFB). Hence the escape

positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The PR intervals(+-+) are variable, indicating AV dissocia-

rhythm is junctional with an RBBB and LAFB. The QT/QTc intervals are prolonged (560/400 msec) but are normal (480/340 msec) when

tion. The atrial rate is faster than the ventricular rate, and hence this is complete heart block. The QRS complexes are wide (0.16 sec) with

adjusted for the increased QRS complex duration.

continue$

249

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Conduction Abnormalities: Cora Case 51

In ECG 51B, there is a regular rhythm at a ventricular rate of 32 bpm. P waves (*) arc seen, and they have a stable PP interval ( U) at an atrial rate of 78 bpm. The PR interval (~~ :m :Li ;:r :n; l:u ·:;: g~: ~t:: ::·~:!~~:~I::~::::::::~: .:g g:~ g t:: :'" ::: :·: •"':. :;f :1•: ,,,. ':': ·'"~ .,,, :':: ":' :•lJ ·~:! "!' lP~ ;:;; :m ,;,: P '"' :.:~ ·~;: ~ :: 11'' !:g !:g ·:1• ,,,, !": '.fli ·::: :•:: ,,, "'' :::• ~::· : ·• ':" •=.:~ ,,,. ·~·· "': ;::: !·t ,,,, ·~: :: ·: :; ·':· :: .. :1. ~~ .-" ·';' :;:: .. ;: . :: .;.?.' -:s:•'" .,. :·" :;:: 'll: ;;;; ~:· ]::: ::;;H.::!"' .. ,. i:l ; ;l'' ::::. :.: ' ,, .·: ~;~ !:'1 ;::; ::~: .::: :::; :;:: : J': :::· Et. 1$ ::;; ::;; n;: ;if !;;; ·!, il. ii ,:,,.,:, If· i·, ::' ;: ; ;:: , : . It ·:r m.:v.1 :::: :g: gg 'iii m~ :g' ~m i~n m: iii~ ;:av ·:!. ,g, ;;;; :m g:: m: ::,; y ·::. ·;·: :~:: •:u~:" · ;~·: ···: =:•: .:.: :::l ":;: ::• .:~ ,,,, .. = : · v. •• '· :·· •::· :i" ::· 1 ;:":: ::;; ";: ;::: :::: :::; :::: 'r:": ;" :t '::. i.:~ :.::: :m :m m: :~:: :;;: ::~: ::: 1·il: a~;; ~,g ,;,~ ;g; g;; l::: g,~ ,: ,g, ,.,; gi: :;g i=; ·==; ij;· =. == 1

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878

Conduction Abnormalities: Practice Case 78

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

In ECG 78B, obtained while the patient was symptomatic, there is a regular rhythm at a rate of 40 bpm. P waves arc seen (+), although some of the P waves are not obvious as they arc within the QRS complexes or on the T waves (A). When the P waves are seen, however, the PP interval is constant ( U) at an atrial rate of 98 bpm. The last P wave (l') is early and has a different morphology: it is a premature atrial complex that is nonconducted. Another premature P wave can be seen immediately before the fourth QRS complex (..l). There is no rdationship between the P waves and the QRS complexes (ie, the PR intervals are variable; +-+). Therefore, AV dissociation is present. As the atrial

The QRS complexes are wide (0.16 sec), and their morphology is unlike that of the QRS complexes in ECG 78A (ie, they have neither a typical right or left bundle branch block morphology). Hence these are ventricular complexes. As would be expected in the presence of hi-bundle branch block, the development of complete heart block is associated with an escape ventricular rhythm. The slow escape ventricular rhythm is very likdy the cause of the patient's symptoms. Hence the insertion of a permanent pacemaker is indicated. •

rate is faster than the ventricular rate, this is complete heart block (or third-degree AV block).

379

75-year-eld woman pre~~ntl to the emergency departmeld wltlt dizziness a•d lteadache. Her lilted preuurela noted to be 220/111 mm Hg. The 01m Ia etherwlse unreMarkable except fer a slow hllrt rate. An EC& Ia obtalllad (71A). She Ia adMitted to the ltoapltal fer severe

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llypartanslan and Initiated on tllarapy wltllan anglatenaln· OGIWtrtlng enzyme (ACE) lnltlllltor, calelum-cha•nel bleeker, and It-blocker. After therapy liar blaad preuure ls1•0/ID mm Hg, and Iter pulse remat111 slew. However, telemetrr sltows a cllante a11d another ECI 11 obtained (711).

What accounts for the slow heart rate? What therapy Is necessary?

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ECG 79A Analpls: lormel alnua riiJihm with ventrtculophlllc arriiJihmla, first-degree AV block (prolonged AY canductlan), 2:1 secand·degree AY lllack, lntraventrlculer canductlan delay

882

Conduction Abnormalities: Practice Case 79

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

ECG 79A shows regular RR intervals at a rate of 36 bpm. There is a P wave(*) before each QRS complex with a stable PR interval (44) of 0.24 second (first-degree AV block or prolonged AV conduction). A second P wave(+) can be seen after each QRS complex. This P wave is nonconducted. The presence of an occasional nonconducted P wave defines second-degree AV block, and there is a pattern of 2:1 AV conduction. The atrial rate is not constant, and the PP interval surrounding the QRS complex ( n) is shorter (0.70 sec) than the PP interval without a QRS complex ( U) (0.84 sec). This represents ventriculophasic arrhythmia. This finding can be seen whenever there is 2:1 AV block or complete heart block. Ventriculophasic arrhythmia is due to enhanced sinus node impulse generation resulting from ventricular contraction. This may be the result of increased sinus nodal artery pulsatile blood flow with ventricular contraction; stretching of the right atrium with ventricular contraction, resulting in an increase

in sinus node automaticity; or baroreceptor changes resulting from the stroke volume occurring with ventricular contraction. The QRS complexes are wide (0.11 sec) but are not wide enough to be a full left bundle branch block (LBBB; ie, they are

not~

0.12 sec).

They do not demonstrate a pattern of a right bundle branch block nor do they have a typical LBBB pattern as there is a terminal S wave in lead V6 (&) representing terminal forces in a leh-to-right direction, which cannot be seen with an LBBB. Hence this is an intraventricular conduction delay (IVCD). There are nonspecific ST-T wave changes (").The axis is leftward, between o• and -30" (positive QRS complex in lead I, biphasic QRS complex in lead II, and negative QRS complex in lead aVF). The QT/QTc intervals are 500/390 msec (460/360 msec when corrected for the prolonged QRS complex duration).

co~ttinue1

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L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

In ECG 79B, there are regular RR intervals at a rate of 34 bpm. The atrial rate is constant ( n) at 72 bpm, and the P waves(*) are positive in leads I, II, aVF, and V4-V5. The PR interval (U) is not constant, and AV dissociation is present. AV dissociation with an atrial rate faster than the ventricular rate indicates complete heart block. The escape rhythm has a widened QRS complex (0.11-0.12 sec) that is almost identical in morphology to that seen in ECG 79A; hence this is an escape junctional rhythm. The slight difference in the QRS morphology of these junctional complexes when compared with the sinus complexes is due to the fact that the junctional complex originates from an ectopic

the AV node. An escape QRS complex that is wide and abnormal is consistent with a ventricular focus and hence the 2:1 AV block is Mobitz type II with infra-Hisian disease. If ECG 79B were the only tracing available, it would be uncertain whether the escape rhythm was junctional with an underlying IVCD or a ventricular rhythm. In this situation an invasive electrophysiologic study would be required to determine the locus of the block. However, as ECG 79A is available and shows that the conducted complexes have the same morphology as the dissociated complexes in ECG 79B, it is clear that this is an escape junctional rhythm.

focus within the AV junction and the impulse it generates enters the bundle of His at a different location when compared with the sinus impulse, which is conducted through the AV node. The difference in conduction pathway through the His-Purkinje system will result in a slightly different morphology, axis, or amplitude.

The 2:1 AV block is a result of underlying AV nodal disease. Severe hypertension can result in a decrease in sympathetic tone and an increase in vagal tone mediated through the baroreceptors and, therefore, can contribute to AV nodal conduction abnormalities. The repeat ECG shows complete heart block with an escape junctional rhythm that

The etiology of the conduction problem with 2:1 AV conduction can

is possibly a result of ~-blocker therapy in the presence of underlying

be established when complete heart block develops; the origin of the escape rhythm indicates whether the block is within the AV node or is infra-Hisian (ie, within the His-Purkinje system). If the escape QRS complex is narrow or similar to the conducted QRS complexes, the 2:1 AV block is Mobitz type I due to conduction abnormality within

AV nodal disease. The first step would be to discontinue the JJ-blocker. If conduction improves, then no further therapy is indicated. However, if complete heart block persists, indicating structural disease of the AV node, then a permanent pacemaker is indicated. •

385

Notes

A

21·year-old woman wHh peralatent carclloMyopat"' following a pregnancy 8 monthlago preunta to her primary care '"'''clan wHh complaints of lntennltttnt palpltatlona. Eplaodaa are unheralded and wHhout any oUter aaaoclated tJmptoma.

She deniH dyapnea. Of note, aymptoma atarted 1 week ago, approximately 2 waek8 after the aelf-dlacontlnued her ,._blocker. She ltatea thlt the •croetn't need tho88 pUla anJiftore.• An ECC Ia obtained during one of her eplaodaa of palpltatlonl.

What Is the cause of the patient's symptoms?

387

Podrld's Real-World ECGs

ECC 80 Analysis: lormal sinus rllythm, first-degree AV block (prolonged A¥ conduction), left bundle branch block, premature ventricular complea, complete heart block with ventricular escape, trifascicular disease

888

Conduction Abnormalities: Practice Case 80

L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __

There is a regular rhythm at a rate of 62 bpm. There is a P wave (*) before the first four QRS complexes (j) with a constant PR interval of 0.24 second (--l

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Conduction Abnormalities: Practice Case 98

with the same duration (2.08 sec). The rhythm is, therefore, regularly irregular. The remaining RR intervals are all the same, at a rate of 58 bpm. The QRS complex duration is normal (0.08 sec) and there is

before the third and fifth QRS complexes UJ. It is likely that the slightly shorter PR interval is the result of slight enhancement of AV conduction due to the longer RR interval (slower rate), which allows for more rapid AV conduction as the AV node has had more time for recovery. During

a normal morphology. The axis is extremely leftward, between -30° and -90" (positive QRS complex in lead I and negative QRS complex in leads II and aVF with an rS morphology). This is a left anterior

each pause there is an on-time P wave (PP intervals are constant) ( U) that does not have a QRS complex following it. Hence this is a seconddegree AV block (ie, an occasional nonconducted P wave). As all of

fascicular block. The QT/QTc intervals arc normal (400/395 mscc). There are P waves (+) before each QRS complex with a stable PR interval (0.28 sec) ( n), except for a slightly shorter PR interval (0.24 sec)

the PR intervals are constant (except for the PR interval after the long pause), this is a Mobitz type II second-degree AV block. The block is, therefore, within the His-Purkinjc system.

In ECG 98A, the rhythm is irregular as a result of two long pauses (..-.)

481

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Conduction Abnormalities: Practice Case 98

ECG 98B shows regular RR intervals at a rate of 44 bpm. However, the second and seventh QRS complexes (T) are early. All the QRS complexes (except for the second and seventh) are wide (0.18 sec), and their morphology resembles that of a right bundle branch block (tall, broad

in ECG 98A. The PR interval associated with these QRS complexes is also identical to the PR intervals seen in ECG 98A. This is, therefore, complete AV block with an escape ventricular rhythm and intermittent capture. The captured complexes are identical to the conducted com-

R wave in lead Vl [--+] and broadS wave in leads I and V5-V6 [+-]).It

plexes seen in ECG 98A. The fact that the dissociated QRS complexes

is, however, not a typical right bundle branch block as there is a tall monophasic R wave in leads V1-V3. There are P waves(*) that have a regular PP interval ( U) at a rate of 60 bpm. Some of the P waves are located within the ST segment(+) and are, therefore, less obvious. However, the P waves that are seen occur at a regular PP interval ( U).

are wider and have a different morphology when compared with the captured complexes, which are narrow and have a normal duration and morphology, indicates that the dissociated complexes are ventricular in origin.

The P waves are positive in leads I, II, aVF, and V4-V6 and hence there is an underlying normal sinus rhythm. The PR intervals are very variable (+-+), and the P waves are dissociated from the QRS complexes.

In this patient with Graves' disease, it would be important to check thyroid status as continued hyperthyroidism may be associated with com-

As the atrial rate is faster than the ventricular rate, there is complete (third-degree) AV block.

plete AV block, although this usually occurs in patients with underlying conduction system disease. When the heart is "stressed" by the hyperthyroid state, complete AV block may become manifest. However, in this situation the sinus rate is likdy to be more rapid than seen on these

As indicated, the second and seventh QRS complexes (T) have a normal

ECGs due to sympathomimetic effects seen with hyperthyroidism.

duration (0.08 sec) and morphology. There is a P wave (") before each, with the same PR interval (n) (0.28 sec). In addition, these two QRS complexes are early, indicating that they are the result of the P wave preceding them. Importantly, the two narrow QRS complexes have the same duration, morphology, and axis as the QRS complexes seen

Nevertheless, if hyperthyroidism was still present, with further therapy there would likely be resolution of the complete AV block. However, the presence of persistent complete AV block (in the absence of hyperthyroidism) associated with an escape ventricular rhythm is an indication for implantation of a permanent pacemaker. •

483

Notes

A n ECG from an IIJIIIptGmatlc

K 24-year-old wemanls preeenttd. 1

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Podrld's Real-World ECGs

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EC6 99 Analysis: Sinusllradycardia, intraventricular conduction delar to the right ventricle

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Conduction Abnormalities: Practice Case 99

The rhythm is regular at a rate of 46 bpm. There is a P wave (*) before each QRS complex with a stable PR interval (0.20 sec). The QRS duration is slightly prolonged (>0.10 but< 0.12 sec), and there is an RSR' complex in lead Vl (o-) and a prominent S wave (i) in

ventricle to right intraventricular conduction delay to pathologic RBBB. The QRS complex width defines the diagnosis. If the QRS complex width is normal (ie, < 0.10 sec), the morphology is deemed a normal variant and is termed a crista pattern. If the QRS complex duration is

leads I and VS-V6. Although the QRS complex morphology is that of a right bundle branch block (RBBB), the QRS complex duration

slightly prolonged (0.10 to 0.12 sec), an intraventricular conduction delay to the right ventricle is present (this is often called an incomplete

is not wide enough for a bundle branch block. This has often been termed an incomplete RBBB, although it is actually a conduction delay to the right ventricle and is best termed an intraventricular conduction delay. The QT/QTc intervals are normal (440/385 msec).

RBBB). If the QRS complex duration is longer than 0.12 second, the diagnosis is complete RBBB.

The RSR' morphology seen in the early (right) precordial leads (ie, Vl-V2) represents a spectrum of physiology ranging from normal delayed depolarization of the crista supraventricularis of the right

In this case, there is an intraventricular conduction delay to the right ventricle. The term incomplete RBBB, often applied to this pattern, is not accurate as the bundle manifests •an or none" conduction characteristics; that is, it either conducts (always at the same rate) or does not conduct. This is not of any clinical importance, although it may be associated with the development of a complete RBBB in the future. •

467 tahir99-VRG & vip.persianss.ir

7t-yaar-old man wltlla hlltary of coronary artery dlaaaaa and a previous MyOcardial Infarction (MI) Is sea• In the •••aency departMent for complalnll crtlntannlttent fatigue 111d llghtllaadedneu that have been occu~r1111 fer the past week. He states tllat tile symptoMs occur episodically, unrelated to actiVIty. Eaclt eplaoda laata for about 30 mlnutea and tllen raaolvaa apontaneaualy. Betwea• the eplaodea he feala wall. Ia came to the

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emergency department •eceuae .r en epllade tllat waa .r lone• duration and usectated with mare severe llghtlleadedness. Hll phplcaleuM ts u•remarkable, except tar a blaad preuure .r 17GIII Mm Hg. An ECIIa obtained (ECG 1tOA). Because he lives alone, It was decided te admH 111m te a telemltry u•lt for obaervatla•. 1111 toltowl•g day he complained at tlglltiiHdednlll, a•d on telemllry there •• a change In hla hHrt rate. An ECI waa obtained (ECI 1001).

What abnormality Is noted on the ECGs? What Is the etiology of the abnormality? What treatment Is Indicated?

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Conduction Abnormalities: Practice Case 100

In ECG lOOA, there is a regular rhythm at a rate of 76 bpm. There is a P wave (+) before each QRS complex with a stable PR interval (0.18 sec). The P wave is positive in leads I, II, aVF, and V4-V6. Hence this is a normal sinus rhythm. The QRS complex duration is increased

There are no Q waves in leads II and aVF; hence the extreme left axis is due to a left anterior fascicular block. There is a deep Q wave in lead V3 and probably in leads V4-V6 W, consistent with an old anterior wall myocardial infarction (MI). The QT/QTc intervals

(0.16 sec), and it has a morphology of a typical right bundle branch block (RBBB), with an RSR' complex in lead Vl (--+)and a broad terminalS wave in leads I and V5-V6 (+-).The axis is extremely left-

are slightly prolonged (400/450 msec) but are normal when the prolonged QRS complex duration is considered (320/360 msec). The

ward, between -30" and -90" (positive QRS complex in lead I and negative QRS complex in leads II and aVF, with an rS morphology).

presence of an RBBB and left anterior fascicular block indicates bifascicular disease. continue$

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Podrid’s Real-World ECGs : A Master’s Approach to the Art and Practice of Clinical ECG Interpretation - Volume 3 - Conduction Abnormalities

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