Clinical Data: 84 years old man diagnosed with unstable angina
Which is the ECG diagnosis?
COMMENTARIES FORUM INTEGRANTS
Dear Andrés
Thanks for this beautiful case.
My interpretation:
1. Junctional rhythm
2. Long QT with big U-waves
3. Flat T-waves with +/- component
ID: Electrolyte Disorder: Hypokalemia (with possible Hypomagnesemia)
Happy New Year!
Dr Baranchuk,Adrian MD FACC
Assistant Professor of Medicine
Cardiac Electrophysiology and Pacing
Director, EP Training Program
Kingston General Hospital
FAPC 3, 76 Stuart Street
K7L 2V7, Kingston ON
Queen's University
Ph: 613 549 6666 ext 3801
Fax: 613 548 1387
barancha@kgh.kari.net
Prof. Dr. Paul Levine considerations
This is a fascinating ECG. I have a different
approach, whether presented with a 12 lead
ECG as in this case or a simple (or
complex) rhythm strip.
In addition to
arriving at a provisional diagnosis which is a
fun intellectual exercise, I try to take this to
the next step and decide on what I would do
for the patient, whether this is simply the
added tests needed to establish a diagnosis
or perhaps, initiate therapy. I have seen this
phenomenon on a repeated basis but more
than 20 years ago when I was active as a
general cardiologist.
I presented an
abstract to the American College of Chest
Physicians in 1989 but never got around to
writing it up for formal publication.
The reference is:
Levine P.A., Klein, M.D., Bradycardia
exacerbated angina, therapy with a combination
of drugs and
pacing, Chest 1989,
134S, Presented at the XVI World Congress on
Diseases of the Chest and 55th Annual Scientific
Assembly, American College of Chest
Physicians, Nov 1, 1989; Boston, MA.
The underlying rhythm is atrial fibrillation (AF).
There is a very slow ventricular
response. There are only 4 cycles that can be measured and these are not absolutely the
same although the variation is minimal. There is at least high grade 2nd degree AV block
although it cannot be characterized as either Mobitz I or Mobitz II in light of the underlying
AF. This is most likely 3rd degree AV block in the presence of chronic AF. Whether the focus
is a junctional escape rhythm or, based on the narrow QRS morphology, a fascicular escape
rhythm, I cannot say without a baseline ECG clearly showing either sinus with intact AV nodal
conduction or AF with a more rapid and more irregular ventricular response to indicate that it
is clearly conducted from the atria.
As to QRS morphology, there is low voltage in the limb leads although not in the precordial
leads. There is an initial "q" wave in Lead V1 and an absence of the expected normal small q
in the lateral leads (D1, aVL, V5-6) raising concerns about a prior septal MI however if the
ventricular escape focus is arising from one of the ventricular fascicles and not the AV node,
any specific diagnosis would be suspect. There is terminal T wave inversion in leads V2-V4
consistent with anterior wall ischemia. There is also a prominent U wave in the anterior
precordial leads which is consistent with the marked bradycardia although I cannot rule out
electrolyte abnormalities or other causes of U waves.
Now to return to my earlier statement and the referenced abstract. I cared for a series
of patients when I was at Boston University Medical Center who presented with the
following scenario. Unstable angina, an increase in beta blockade or calcium channel
blocking therapy was associated with a significant slowing of the heart rate which
caused anxiety on the part of the physicians caring for the patient and was associated
with a worsening of the angina.
The medications (either a calcium channel blocker and/or a beta blocker) were discontinued,
the heart rate increased and at faster heart rates the patient also experienced angina. We
finally implanted a pacemaker (usually a dual chamber although in a patient such as the subject
of this challenge, I would have chosen a single chamber ventricular pacemaker) to prevent the
rate from getting too slow while allowing us to increase the beta blocker and/or calcium channel
blocker with a marked clinical improvement.
My patients had one other factor directing our approach. The patients were not candidates for
coronary artery bypass surgery because of the extent of the coronary artery disease based on
coronary angiography or their general medical status condition precluded major open heart
surgery. Please remember that this was more than 20 years ago and some of those patients
might be a candidate for surgery or another intervention today.
In the management of ischemic heart disease we routinely use medications to slow the
ventricular rate in an effort to reduce the metabolic demand thus restoring a balance between
myocardial blood supply and myocardial oxygen demand. In my patients and this case, the
presenting heart rate was too slow and although the metabolic demand was reduced, the
ischemia actually increased again due to an imbalance between supply and demand. The
hypothesis was based on the fact that the majority of coronary blood flow occurs during
diastole. In a patient with high grade obstructive lesions in the coronary arteries (at Boston
University in the late 1980's we had started doing coronary artery angioplasty. As part of our
own learning curve, we advanced very thin catheters into the coronary arteries and measured
the gradient across the obstructing plaque.)
The gradient across a stenotic lesion was commonly > 50 mm Hg and not uncommonly above
100 mm Hg. With a long diastolic filling period associated with a marked bradycardia, the
diastolic pressure would fall below the required perfusion pressure and the segment of the
myocardium distal to the obstructing lesion would have no perfusion during systole and again
during late diastole creating a mismatch between supply and demand. As such, even with a
slow rate, the net effect was an increase in ischemia and anginal symptoms.
By increasing the rate using pacing therapy, I was able to improve myocardial perfusion while
not further increasing metabolic demand.
I have tried to diagram this but would ask your indulgence for my hand-drawn diagram. Knowing
that cyberspace sometimes markedly distorts diagrams, both a word and pdf file of the same
diagram is attached.
There is also one additional consideration. When treating AF, I used to try to push for rates
similar to a normal resting sinus rate. When invited to give a presentation on the limitations of
the Automatic Mode Switch algorithm at Dr. Santini's conference in Rome in 1996, I discovered
a very interesting phenomenon that has changed the way that I practice with respect to
controlling the ventricular response to AF. I now aim to have a resting ventricular rate around
80-90 bpm. A copy of this book chapter is attached. For that presentation, I extracted the data
presented in the paper by Resnekov and McDonald (1971) and reformatted it as sinus rhythm
vs AF with respect to cardiac output. For similar cardiac outputs, the sinus rate is, on average
20 - 40 bpm slower than the rate in AF. The extrapolation to what I had always considered the
desired resting rate in a patient with chronic AF actually resulted in a low cardiac output state
which doesn't help coronary perfusion or perfusion of the other organs in the body.
The patient whose ECG was circulated has an even slower rate so I suspect a marked
decrease in cardiac output and a serious limitation to coronary perfusion.
1
1.
Resnekov L, McDonald L. Electroversion of lone atrial fibrillation and flutter including haemodynamic studies at rest and on exercise. Br Heart
J. 1971 May; 33: 339-350.
The benefit of a higher (paced) rate during AF was subsequently shown by Brunner-La Rocca
and colleagues utilizing a metabolic stress test. These studies were performed in patients with a
DDD pacemaker during automatic mode switch in the presence of AF.
Brunner-La Rocca HP
1
When pacing is involved, maintaining a higher base rate in the setting of a poorly controlled
ventricular response also helps to stabilize the ventricular rate by the mechanism of concealed
retrograde conduction into the AV node.
1.
Brunner-La Rocca HP, Rickli H, Weilenmann D, Duru F, Candinas R. Importance of ventricular rate after mode switching during low intensity
exercise as assessed by clinical symptoms and ventilatory gas exchange. Pacing Clin Electrophysiol. 2000 Jan;23: 32-39.
Below is the data presented by Chudzik and colleagues at Europace in 2001.
Dear Dr. Levine, this reference (Chudzik M, et al) it is not in PubMed?
When I attempted a higher base rate in my patients with AF who basically had intact AV nodal
conduction, the following is an example:
To return to the 84 year old man with unstable angina, he has AF with a very slow ventricular
response, possibly complete heart block. I propose that the very slow ventricular response is
contributing to his unstable angina and based on the ECG, there is, at least, anterior wall
ischemia. While the preferred management would be revascularization, he might still require
permanent pacing. If he is not a candidate for revascularization, pacing may be of additional
benefit and if the lead is placed in the RVOT, there should be minimal distortion of the paced
QRS complex.
Paul A. Levine MD, FHRS, FACC, CCDS
Vice President, Medical Services
St. Jude Medical CRMD
Tel: 1-818-493-2900 Fax: 1-818-362-2242
plevine@sjm.com
Schematic Diagram
bradycardia:
of
Increase
Ischemia
associated
with
Normal Heart Rate and Coronary Perfusion in the absence of CAD
mm Hg pressure
Diastole –
Period of
coronary
perfusion
120
60
30
Period of coronary
perfusion
Systole Virtually
no
perfusion
Critical coronary perfusion
pressure in normal
Please excuse my attempt at a hand-drawn diagram.
Impact of bradycardia on coronary perfusion in a patient with high
grade coronary artery disease:
mm Hg pressure
120
60
30
Period of myocardial
perfusion
Systolic pressure
Critical coronary
perfusion pressure
Diastolic pressure
No
perfusion
during
systole
No perfusion during
late diastole as
aortic pressure has
fallen below the
critical coronary
perfusion pressure
a
Hola amigos: Mi participación en esta excelente Lista es rutinariamente como "lector", ya que
no soy arritmólogo, sino cardiólogo clínico.Y ,como tal, me voy a animar a opinar, no tanto sobre
la arritmia en sí ( destacados colegas ya han opinado), sino sobre la impresión general que
tengo al ver este hermoso ECG:
a -Ritmo "lento", regular, con ondas “f” de FA en V1.
b -En las derivaciones del PF bajo voltaje, con un eje eléctrico no bien determinado.
c - En V1,comienzo con q, y bloqueo de rama derecha.
d - Diferencia de voltaje entre V1 y V2 (señal indirecto de sobrecarga auricular derecha?).
e -La repolarización en cara anterior, con elementos compatibles con "repolarización no
homogénea" y/o cardiopatía isquémica. (QT largo, ondas T +/- y -/+ ).
Y en el PF la "casi ausencia) de ondas T.
f -Persistenia de ondas S llamativas en V5 y V6
Mi primera impresión "clinico-ECG ?": Puede tratarse de un paciente con EPOC con sobrecarga
derecha, + FA crónica + bloqueo AV, tratado crónicamente con amiodarona, y,
consecuentemente, algún grado de hipotiroidismo por la droga, + cardiopatía isquémica.
Gracias por permitirme opinar (total, mañana termina el 2009, y dejenme el derecho a
equivocarme.... ),
Y Feliz Año Nuevo a todos!!, y en especial al Potro y a Edgardo.
Un abrazo,
Dr Mario A. Heñin
Moderador de coronary-PCVC
Resistencia, (Chaco)
Argentina.
Mi impresion diagnóstica es FA con BAV completo y ritmo del haz de Hiz. SCA con QT
prolongado.
En el ECG del paciente de 84 años:
1. No visualizo ondas P, si una linea de base en serrucho en V1 y V2 que podria
corresponderse con una FA, como el rtimo ventricular es regular de 53 latidos minutos (eso
es lo que logro medir). Interpreto con respecto a esto que se trata de una FA con BAV
completo y un ritmo nodal o del haz de His.
2. Digo esto porque el QRS no se encuentra desviado ni con aumento del tiempo de
conduccion. Me gustaria conocer la opinion de los especialistas acerca del eje electrico y
las s profunas en V5 y V6.
3. Intervalo Qt prolongado, en paciente con síndrome coronario agudo. El QTc lo estimo en
560 mseg. No se refiere sintomatologia como debilidad muscular etc que me puedan hacer
pensar en un trastorno electrolitico como causa de la prolongacion del QT.
3. Presenta transtornos de la repolarizacion en las derivaciones de V2 a V4.
4. Presenta onda U en las mismas derivaciones.
Creo se trata de una FA con BAV completo, en el contecto de un paciente de 84 años con
un Síndrome coronario agudo. Ya que el paciente segun refieren en el envio del ECG tiene
angor. Me gustaria saber los valores enzimaticos de marcadores de isquemia cardiaca.
Obviamente ayudaria en las conductas a seguir. Desconozco porque en los datos enviados
si se encontraba tomando medicamentos que puedan provocar BAV, ya que si padecia
previamente de FA probablemenete estuviera tomando BB, amiodarona, o algun
medicamento para esto.Si estaba tomando medicamentos bradicardizantes y las enzimas
cardiacas son normales, se podria tomar la decision de tomar una conducta espectante y
medicar para su Síndrome coronario agudo.
En el caso de no estar tomando medicamentos de este tipo previos, se podria evaluar la
colocacion de un marcapasos transitorio y conducta espectante de acuerdo a evolucion. Y
luego con los estudios diagnóstico de Ecodoppler (digo ecodoppler porque permite valorar
todo lo que ya conocen todos acerca de la utilidad del eco para la evaluacion de Smes
coronarios Agudos y a mi juicio el doppler siempre brinba informacion adicional
complementaria interesante, funcion diastolica y en este caso en particular observar la
ausencia de onda E lo que confirmaria el dianostico de FA y tambien me permite estimar el
volumen minuto no solo la Fey. ya que en este paciente en particular el angor podria
corresponder a un BAV completo con bradiacaria sinusal e hipoflujo y angor secundario a
esto.
Si presenta alteraciones de la motilidad en el ecocardiograma o marcadores enzimaticos
cardiacos positivos, evaluar de acuerdo a evolucion y respuesta al tratamiento CCG. Esto
de acuerdo al riesgo de arritmias en el contexto de un paciente con QT prolongado en el
contexto de un IAM.
1.
2.
S. Ahnve QT Interval Prolongation in Acute Myocardial Infarction European Heart Journal Advance Access published on November 2,
1985, DOI 10.1093/eurheartj/6.suppl_D.85.Eur Heart J 6: 85-95.
Paventi, Saverio, Bevilacqua, Umberto, Parafati, Maria A., Di Luzio, Enza, Rossi, Francesco, Pelliccioni, Patrizia R., Paventi, Saverio. QT
Dispersion and Early Arrhythmic Risk During Acute Myocardial Infarction Angiology 1999 50: 209-215
Martin Ibarrola M.D.
Dear Dr Paul Levine I would like to discuss the very interesting case of al old man with
angina. I agree with your approach related to intractable angina syndrome with severe
bradycardia. This ECG ,is probably a non coronary disease patient. As you remarked in your
discussion the ECG shows small limb complexes, but with large one in the precordial leads.
In clinical practice
this pattern very frequent indicates left ventricular hypertrophy and
dilatation mostly is very extensive transmural anterior myocardial infarction with deep S
waves in right precordial leads
I suspected that this case is a hypertrophic cardiomyopathy witch evolved to dilatation
the atrial flutter /fibrillation seen in V1 is aquencense in all other leads suggesting a long
standing AF in a severe fibrotic and dilated left atrium
The second problem is the severe impaired conduction delay in the upper node and in the
infranode junctional tissue
This pattern is not observe in chronic ischemic syndrome . Why ?
Because this area is supply by all 3 arteries
1) From the right coronary in 80% of the cases
2)The infranodal is suplied by the circumflex and the first ramus of septal arteries
this tissue is very important to regulate de heart rate toward the ventricle . mather nature give
not over flow to any tissue in the heart , but almost only to the sinus node and to the AV node
coronaries event
cannot destroy these tissues as occur in active myOcites
and
intraventricular conduction system
I think that a primary disease affect these two areas.
The ventricular area is also severely affected the wideness of V3 isabout 120ms, indicating
most probably a severe intraventricular conduction delay
The inverted waves seen in right precordial leads is the junction between the T and U waves
in a case of an octagenarium patient in whitch the ECG shows all the cardiac areas (atrium ,
supra and infanode AV nodes and the LV as well. The first clinical diagnosis is infiltrative
disease,probably amiloidosis
Why amiloidosis ?
Because this infiltrative heart disease has the biological mechanism as alzmhier
in the hypertrophioc heart there are an hyperproduction of protiens, about 50% of the proteins
are imperfect structured or unfolded( see cardiovascular research January 2010 )
There are a series of proteins that destroy the miss folded
The first line are the chaperones , second line ubiquitine ׂ (Nobel award 2007) the third line
are the proteosome
This system avoid the entrance of miss folded protein to the myocytes, but is the production
is very high or defender system is exausted the imperfect protein enter in the
sarcomeres
The angina could be provoked by tha suffocated microcirculation due to the fibrotic
extracelular matrix
the only study I recommend is mri , witch can help for the diagnosis
I agree with your therapeuticall approach
MY KINDLY REGARD AND HAPPY NEW YEARS
Samuel Sclarovsky
Our ECG diagnosis
•
Atrial fibrillation (AF) with slow ventricular response about 48bpm. presence of an irregularly
irregular rhythm in the absence of P waves. Undulations in the baseline ("f waves") are
present mainly in V1
•
QRS axis is hard to determinate, but clearly positive in III and aVF and isodyphasic in aVR:
near +120 degree
•
Anteroseptal ischemia: it is an example of Type 1 Wellens´ warning “Plus-minus” in V2-V3
and “minus-plus” in V4
•
Low QRS voltage only in limb leads
•
Minuscule qs complex in V1: The R wave may be absent in lead V1, and qs complex is
recorded1. A qs deflection, however, is rare in lead V21. Eventually, correspond to Peñaloza
and Tranchesi sign: QRS complexes of low voltage in V1 contrasting with QRS complexes of
normal voltage or increased in V2. This is an indirect ECG criteria of right atrial enlargement.
If we considered that the QRS axis is located in +120 degree, right ventricular
enlargement/hypertrophy (RVE/RVH) diagnosis is possible.
1.
Surawicz B, Knilans TK. CHOU´S ELECTROCARDIOGRAPHY IN CLINICAL PRACTICE Adult and Pediatric SIXTH EDITION SAUINDERS
ELSERVIER 2008. SECTION 1 Normal ECG pp:16.
Minimally Irregular HR > AF
“f waves”
“Plus-minus T waves”
HR = 55bpm HR = 48bpm HR = 51bpm
QRS axis + 120 degree? *
Low voltage of QRS complexes only in limb leads
“Minus-Plus- T waves”
* QRS positive only in III and aVF: QRS axis near +120 degree
Clinical Data: 84 years old man diagnosed with unstable angina
HEART RATE (HR) = 48bpm
PROLOGED QT INTERVAL
QT = 680ms
Mean Predicted QT Values according to RR Cycle Lengths for man
1.
RR (ms)
HR (bpm)
Mean Value
Lower Limit
Upper Limit
125
48
414ms
370ms
458ms
Sagie A, Larson MG, Goldberg RJ, Bengtson JR, Levy D. An improved method for adjusting the QT interval for heart rate (the Framingham
Heart Study) Am J Cardiol. 1992 Sep 15;70:797-801.
The QTc interval estimation is performed also by applying the Bazett’s formula
proposed in 1920:
measured QT
QTc =
RR
Besides sex, the age also influences QT interval duration.
Prof. Dr. Arthur Moss, from the University of Rochester, New York, at the 50th
Annual Session of Specialists of the American College of Cardiology, 2001 in
Florida, Orlando, highlighted the fact that in those affected with congenital LQTS,
the QTc interval may be normal or in borderline values (< 450 ms).
DIFFERENTIATION OF BIMODAL OR
NOTCHED T WAVES WITH T-U INTERVAL
Bimodal or notched T waves may be distinguished from the T-U interval: the second
apex of bimodal T wave (T2) is at a distance from the first one (T1) < 150 ms; the T1U interval is > 150 ms 1-2.
> 150ms
< 150ms
T1
T2
BIFID
ONDATTWAVE
BÍFIDA
U
The second apex of bimodal T wave (T2) is at a distance < 150 ms from the first
module (T1): The T1-U interval is always > 150 ms.
1.
2.
Lepeschkin E.: Physiologic basic of the U wave. In Advances in Electrocardiography. Edited by Schlant RC, and Hurst JW. New York,
Grune & Stratton 1972;pp 431-447.
Lepeschkin, E.:The U wave of the electrocardiogram. Mod Concepts Cardiovasc Dis 1969;38:39.
Wellens´ syndrome type 1: biphasic T waves “plus-minus” in leads from V2 an V3
•
•
•
•
•
•
The T-wave abnormalities are persistent and may remain in place for hours to weeks
History of unstable angina chest pain without serum marker abnormalities:
Little or no enzyme and troponin elevation
Absence of changes in the QRS complex within 24hours(the Wellens sign)
Minimaly elevated or isoelectric ST segments
The ECG finding was strongly associated with significant stenosis in the LAD.
Commentaries
Prevalence of AF increases dramatically with age. The prevalence of AF among persons ≥
80 years is near 10%1. AF is caused by multiple reentrant waveforms within the atria,
which bombard the AV node, commonly leading to a tachycardia that is irregularly
irregular. There is loss of atrial contraction and its contribution to ventricular filling, also
referred to as loss of atrial kick. In addition, this loss of contraction can lead to stagnation
of blood in the atrium and can promote thrombus formation. Patients may be at risk for
embolization when AF converts to sinus rhythm as organized atrial contractions can now
cause the dislodging or fragmentation of the atrial thrombus into the systemic circulation.
The rate at which AF causes a ventricular contraction is dependent upon the refractory
state of the AV node.
1. A rapid ventricular response, if the rate averages over 120 beats/minute.
2. A controlled (moderate) ventricular response, if the rate averages between 70-110
beats/minute.
3. A slow ventricular response, if the rate averages less than 60 beats/minute. This is
our case.
1.
Benjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the
Framingham Heart Study. Circulation. Sep 8 1998;98:946-952.
Sick Sinus Syndrome1 (SSS), also called sinus node dysfunction, is a group of
arrhythmias presumably caused by a malfunction of the SA node and subsidiary
pacemakers. Bradycardia-tachycardia syndrome is a variant of SSS in which slow
arrhythmias and fast arrhythmias alternate. Cardioinhibitory and vasodepressor forms of
SSS may be revealed by tilt table testing.
Holter monitoring may be necessary because arrhythmias are transient2.
The ECG may show any of the following: Inappropriate sinus bradycardia, sinus arrest,
sinoatrial block, AF with slow ventricular response, a prolonged asystolic period after a
period of tachycardias, atrial flutter, ectopic atrial tachycardia, sinus node reentrant
tachycardia.
Electrophysiologic tests are no longer used for diagnostic purposes because of their low
specificity and sensitivity.
1.
2.
Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome.
Circulation. 2007 Apr 10; 115: 1921-1932.
Adán V, Crown LA. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician. 2003 Apr 15; 67:1725-1732.
Low QRS voltage only in limb leads: Causes and
mechanisms
Low QRS voltage on the 12-lead surface ECG is present when the amplitude of all six standard
limb leads is less than 5 mm1. (1 large square or 5 small squares, vertically) and ≤ 10 mm in all
precordial leads2. This finding may be a normal variant, but necessitates investigation of the patient
for an underlying cause.
ECGc low QRS voltage has many causes, which can be differentiated into those due to the heart's
generated potentials (cardiac) and those due to influences of the passive body volume conductor
(extracardiac)3. A variety of cardiac and systemic diseases may be responsible. The clinical
correlate of an ECG with low voltage in the limb leads but normal precordial QRS amplitudes is
unclear. Low voltage isolated to the limb leads is associated with the same conditions that cause
diffuse low voltage in only half of patients. In the remainder, more than 60% have dilated
cardiomyopathies. Fifty-one of 100 patients had voltage discordant ECGs that correlated with
conditions known to cause diffuse low voltage. Among those without associated conditions, 63%
had dilated ventricles, with an average ejection fraction of 33%(2).
Peripheral edema of any conceivable etiology induces reversible low QRS voltage , reduces the
amplitude of the P waves and T waves, decreases the duration of P waves, QRS complexes, and
QT intervals, and alters in turn the measurements of the SA-ECG and T wave alternans, all with
enormous clinical implications3.
1.
2.
3.
Berk WA Clinical implications of low QRS complex voltage. J Emerg Med. 1987 Jul-Aug;5:305-310.
Chinitz JS, Cooper JM, Verdino RJ.J Electrocardiol. 2008 Jul-Aug;41(4):281-6. Epub 2008 Mar 19.Electrocardiogram voltage discordance:
interpretation of low QRS voltage only in the limb leads.
Madias JE. Low QRS voltage and its causes. Electrocardiol. 2008 Nov-Dec;41:498-500.
“ The Goldeberg ECG sign”
Idiopathic Dilated cardiomyopathy (DCM) is associated with high QRS voltage in precordial
leads but a decrease QRS voltage in limbs.
To study this paradoxical relationship further, ECGs were retrospectively analyzed by
Godberger et al1 from five groups of men.
Frontal plane QRS voltage was computed as the sum of peak-to-trough QRS amplitudes in
the two limb leads with highest QRS voltage; precordial QRS voltage as the maximum peakto-trough QRS voltage in leads [V1 or V2] + [V5 or V6].
The precordial/frontal plane QRS voltage ratio was significantly greater in 26 patients with
idiopathic DCM compared to 29 patients with compensated aortic valve disease, 30 healthy
men and 20 patients with ischemic heart disease and relatively normal left ventricular
function, but not significantly different from the ratio for patients with ischemic
cardiomyopathy. This differential effect of DCM on precordial and frontal plane QRS voltages,
which probably relates to a combination of mechanical and vectorial factors, may be the basis
of a useful new ECG sign. Others research confirmed these observations2;3.
1.
2.
3.
Goldberger AL, Dresselhaus T, Bhargava V. Dilated cardiomyopathy: utility of the transverse: frontal plane QRS voltage ratio. J
Electrocardiol. 1985 Jan;18:35-40.
Glancy DL, Jones BR, Raven MC, FitzPatrick JA. ECG of the month. Repeated hospitalizations for dyspnea and edema. Dilated
cardiomyopathy. J La State Med Soc. 2006 Jul-Aug;158(4):165
Glancy DL, Newman WP.Atrial fibrillation with QRS voltage low in the limb leads and high in the precordial leads. Proc (Bayl Univ Med
Cent). 2008 Oct;21:437-438.
POSSIBLES CAUSES OF LOW QRS VOLTAGE
I) CARDIAC CAUSES
II) EXTRACARDIAC CAUSES
Due to the heart´s generated potentials
1) Myocardiosclerosis
2) Cardiomyopathies
3) Extensive Myocardial Infarctions
4) Cardiac
Primary
hemochromatosis1. depression of
ST segment and inversion of T
waves in I, II, III, aVF, and V4-6.
associated to low QRS voltage
5) Dextrocardia: low voltage in
precordial leads V4 through V6.
Due to influences of the passive body volume conductor
1) Normal variant2
2) Feminine gender with gigantomastia: in women the
breasts push away the electrodes from the heart.
3) Obesity3.
4) Edematous states: peripheral edema anasarca:
Transient low-voltage ECG4.
5) Pleural, pericardial, or pleuro-pericardial effusion
6) Constrictive pericarditis
6) Left pneumothorax
7) Hypothermia5
8)
Pulmonary
emphysema/Chronic
obstructive
6
pulmonary disease (COPD) . by increase resistivity of
the lung7.
9) Mitral stenosis
Kurabayashi H, Kubota K, Tamura J, Yanagisawa T, Shirakura T. Correlation between the depth of inverted T waves and the serum level of ferritin
in a deferoxamine-treated patient with primary hemochromatosis and hyperthyroidism. Jpn J Med.1989 Mar-Apr;28:243-246.
Berk WA. Clinical implications of low QRS complex voltage. J Emerg Med. 1987 Jul-Aug; 5: 305-310.
da Costa W, Riera AR, Costa Fde A, Bombig MT, de Paola AA, Carvalho AC, Fonseca FH, Luna Filho B, Póvoa R.Correlation of electrocardiographic
left ventricular hypertrophy criteria with left ventricular mass by echocardiogram in obese hypertensive patients. J Electrocardiol. 2008 NovDec;41:724-729.
Madias JE. Reversible attenuation of voltage of QRS complexes and P waves and shortening of QRS duration and QTc interval consequent to large
perioperative intravenous fluid infusions. J Electrocardiol.2006 Oct;39:415-418.
de Souza D, Riera AR, Bombig MT, Francisco YA, Brollo L, Filho BL, Dubner S, Schapachnik E, Povoa R. Electrocardiographic changes by
accidental hypothermia in an urban and a tropical region. J Electrocardiol. 2007 Jan;40:47-52.
Spodick DH. Pulmonary emphysema: classic, quasi-diagnostic ECG. Am J Geriatr Cardiol. 2006 May-Jun;15:193
Baxley WA, Dodge HT, Sandler H. A quantitative angiocardiographic study of left ventricular hypertrophy and the electrocardiogram. Circulation.
1968 Apr;37:509-517.
III) MIXED CAUSES
1. Amyloidosis: pleural and pericardial effusions (extracardiac) and
subendocardial infiltration with amyloid protein1.
widespread
2. Myxedema: It is caused by pericardial effusion, increased skin resistance (external
causes), vacuolated degeneration and fibrosis(intrinsic or cardiac causes)2.
3. Systemic lupus erythematosus: Secondary to interstitial fibrosis, infiltration with
inflammatory cells, predominantly lymphocytes, and plasma cells, interstitial
myocarditis(cardiac causes) and eventually pericardial effusion3 (extracardiac cause).
1.
2.
3.
Cheng AS, Banning AP, Mitchell AR, Neubauer S, Selvanayagam JB. Cardiac changes in systemic amyloidosis: visualisation by magnetic
resonance imaging.Int J Cardiol. 2006 Oct 26;113:E21-23.
Fujimoto K, Tagata M, Nagao M, Suzuki Y, Iida H, Kageyama F, Yoshitomi A, Hirose S, Ikegaya H, Okano H, et al. A case of myxedema heart
with serial endomyocardial biopsyKokyu To Junkan. 1992 Oct;40:1019-1023.
Takahashi T, Suzuki T, Suzuki A, Yamada T, Koido N, Akizuki S, Matsuoka Y, Irimajiri S, Fukuda J.A case of systemic lupus erythematosus with
interstitial myocarditis leading to sudden deathRyumachi. 1999 Jun;39:573-579.
DETERMINANT FACTORS OF QRS VOLTAGE1
1. Number of cardiomyocytes: directly proportional2.
2. Cardiomyocytes Size (cell radius)3
3. Intercalar disc number: directly proportional4
4. Left Ventricular mass: directly proportional5.. This parameter has a good correlation
with the QRS voltage6.
5. Left ventricular surface area and greater wall thickness: directly proportional. This
parameter has a very weakly correlation with QRS voltage. For a given LVM, ECG
voltage criteria of LVH are independent of LV chamber dilatation or other geometric
variables, but depend on age, weight and LV depth in the chest, suggesting that
stratification of subjects by clinical variables has promise for improved ECG
recognition of LVH6.
1.
2.
3.
4.
5.
6.
Surawicz B. ELECTROPHYSIOLOGIC BASIS OFECG AND CARDIAC ARRHYTHMIAS. Silliams&Wilkins 1995; Chapter 26 ABNORMAL
DEPOLARIZATION: ENLARGEMENT AND HYPERTROPHY PP535-548.
Linzbach AJ. Heart failure from the point of view of quantitative anatomy. Am J Cardiol. 1960 Mar;5:370-382.
Thiry PS, Rosenberg RM, Abbott JA. A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.
Circ Res. 1975 Jan;36:92-104.
Toyoshima H, Park YD, Ishikawa Y, Nagata S, Hirata Y, Sakakibara H, Shimomura K, Nakayama R. Effect of ventricular hypertrophy on
conduction velocity of activation front in the ventricular myocardium. Am J Cardiol. 1982 Jun;49:1938-1945.
Wollam GL, Hall WD, Porter VD, Douglas MB, Unger DJ, Blumenstein BA, Cotsonis GA, Knudtson ML, Felner JM, Schlant RC. Time course
of regression of left ventricular hypertrophy in treated hypertensive patients.Am J Med. 1983 Sep 26;75:100-110.
Devereux RB, Phillips MC, Casale PN, Eisenberg RR, Kligfield P. Geometric determinants of electrocardiographic left ventricular
hypertrophy. Circulation. 1983 Apr;67:907-911.
6. Intracavitary blood volume (chamber size): directly proportional. The correlation is not
as good as the correlation with the LV mass
7 Closer proximity of left ventricle to the chest wall: directly proportional.
8. Age: children and adolescents have higher voltage consequence of thin chest
9. Chet diameter: inversely proportional
10. Body build: inversely proportional to Ponderal index (calculated as a relationship
between height and mass.)
11. Ethnic group: higher in afro-descendent men
12. Gender: men > women
13. Hematocrit: directly proportional by change of blood resistivity
14. Bundle branch block: cause diminution of QRS voltage.
15. Changes in respiration or HR.
1.
Surawicz B. ELECTROPHYSIOLOGIC BASIS OFECG AND CARDIAC ARRHYTHMIAS. Silliams&Wilkins 1995; Chapter 26
ABNORMAL DEPOLARIZATION: ENLARGEMENT AND HYPERTROPHY PP535-548.
HAPPY NEW YEAR FOR ALL!
Andrés