https://en.ecgpedia.org/api.php?action=feedcontributions&user=195.229.242.57&feedformat=atom
ECGpedia - User contributions [en]
2024-03-19T06:09:07Z
User contributions
MediaWiki 1.39.5
https://en.ecgpedia.org/index.php?title=ST_Morphology&diff=5643
ST Morphology
2007-12-26T05:25:06Z
<p>195.229.242.57: acelricoloc</p>
<hr />
<div>litrocolo<br />
monchizel<br />
{{nav|<br />
|previouspage=QRS morphology<br />
|previousname=Step 6: QRS morphology<br />
|nextpage=Compare_the_old_and_new_ECG<br />
|nextname=Step 7+1: Compare with previous ECG<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= <br />
}}<br />
==The Normal ST segment==<br />
The ''ST segment'' represents the ventricular repolarisation. Repolarisation follows upon contraction and depolarisation. During repolarisation the cardiomyocytes elongate and prepare for the next heartbeat. This process takes much more time than the depolarisation. Repolarisation is not passive elongation by stretch, it is an active process during which energy is consumed. On the ECG, the repolarisation fase starts at the junction, or ''j point'', and continues until the ''T wave''. The ST segment is normally at or near the baseline.<br />
<br />
The ''T wave'' is usually concordant with the QRS complex. Thus if the QRS complex is positive in a certain lead (the area under the curve above the baseline is greater than the area under the curve below the baseline) than the T wave usually is positive too in that lead. Accordingly the T wave is normally upright or positive in leads I, II, AVL, AVF and V3-V6. The T wave is negative in V1 and AVR. The T wave flips around V2, but there is some genetical influence in this as in Blacks the T wave usually flips around V3.<br />
<br />
The T wave angle is the result of small differences in the duration of the repolarisation between the endocardial and epicardial layers of the left ventricle. The endocardial myocytes need a little more time to repolarise (about 22 msec). This difference causes an electrical current from the endocardium to the epicardium, which reads as a positive signal on the ECG.<cite>braunwald</cite><br />
<br />
==ST elevation==<br />
[[Image:stelevatie_en.png|thumb|ST elevatie is measured 1,5 or 2mm (=60ms or 80ms) after the junctional or j-poin.<cite>Gibbons</cite>]]<br />
[[Image:normal_ST_elevation.png|thumb|Examples of normal ST elevation]]<br />
[[Image:pathologic_ST_elevation.png|thumb|Examples of pathologic ST elevation. [[LVH]], [[LBBB]], [[Pericarditis]], [[Hyperkalemia]], [[Anterior AMI]] ]]<br />
The most important cause of '''ST elevation''' is '''acute [[Ischemia]]'''. Other causes are <cite>Wang</cite><cite>Werf</cite>:<br />
*[[Clinical Disorders#Pericarditis|Acute pericarditis]]: ST elevation in all leads except aVR<br />
*[[Pulmonary_Embolism|Pulmonary embolism]]: ST elevation in V1 and aVR <br />
*[[Clinical Disorders#Hypothermia|Hypothermia]]: ST elevation in V3-V6, II, III and aVF<br />
*[[Clinical Disorders#Hypertrophic_Obstructive_Cardiomyopathy|Hypertrophic cardiomyopathy]]: V3-V5 (sometimes V6)<br />
*[[Electrolyte Disorders|High potassium (hyperkalemia)]]: V1-V2 (V3)<br />
*[[Clinical Disorders#ECG_changes_after_neurologic_events|During acute neurologic events:]] all leads, primarily V1-V6<br />
*Acute sympathic stress: all leads, especially V1-V6<br />
*[[Brugada syndrome]].<br />
*[[Ischemia#Cardiac_Aneurysm|Cardiac aneurysm]].<br />
*[[Miscellaneous#Cardiac contusion|Cardiac contusion]]<br />
*[[Chamber_Hypertrophy_and_Enlargment|Left ventricular hypertrophy]]<br />
*[[Idioventricular Rhythm|Idioventricular rhythm]] including [[Pacemaker|Paced rhythm]]<br />
{{clr}}<br />
<br />
==ST depression==<br />
The most important cause of ST depression is [[Ischemia]]. Other causes of ST depression are:<br />
<br />
*Reciprocal ST depression. If one leads whos ST elevation than usually the lead 'on the other site' shows ST depression. (this is mostly seen in [[ischemia]] as well.<br />
*Left [[Chamber_Hypertrophy_and_Enlargment|ventricular hypertophy]] with "strain" or depolarization abnormality<br />
*[[Miscellaneous#Digoxin|Digoxin]] effect <br />
*[[Electrolyte_disturbances|Low potassium / low magnesium]]<br />
*Heart rate induced changes (post tachycardial)<br />
*[[Clinical Disorders#ECG_changes_after_neurologic_events|During acute neurologic events]].<br />
<br />
==T wave changes==<br />
The T wave is quite 'labile' and longs lists of possible causes of T wave changes exist. A changing T wave can be a sign that 'something' is abnormal, but it doesn't say much about the severity. T waves can be peaked, normal, flat, or negative. Flat and negative T waves are defined as:<br />
<br />
;flat T wave: < 0.5 mm negative or positive T wave in leads I, II, V3, V4, V5 or V6<br />
;negative T wave: > 0.5 mm negative T wave in leads I, II, V3, V4, V5 or V6<br />
<br />
A concise list of possible causes of T wave changes:<br />
*[[Ischemia|Ischemia and myocardial infarction]]<br />
*[[Miscellaneous#Pericarditis|Pericarditis]]<br />
*[[Miscellaneous#Myocarditis|Myocarditis]]<br />
*[[Miscellaneous#Cardiac contusion|Cardiac contusion]] <br />
*[[Miscellaneous#ECG_changes_after_neurologic_events|Acute neurologic events]], such as a subarachnoid bleed.<br />
*[[w:Mitral_valve_prolapse|Mitral valve prolapse]]<br />
*[[Miscellaneous#Digoxin|Digoxin effect]]<br />
*Right and left [[Chamber_Hypertrophy_and_Enlargment|ventricular hypertrophy]] with strain<br />
<br />
==References==<br />
<biblio><br />
#Gibbons pmid=12356646<br />
#Wang pmid=14645641<br />
#Werf pmid=12559937<br />
#braunwald isbn=0808923056<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Junctional_Arrhythmias&diff=5642
Junctional Arrhythmias
2007-12-26T05:24:31Z
<p>195.229.242.57: pastrricr</p>
<hr />
<div>bozelc<br />
trbocdomt<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
*[[AVNRT]]<br />
*[[AVJT|AV junctional tachycardia]]<br />
*[[Nodal Rhythm]]<br />
*[[Idioventricular Rhythm]]<br />
*[[Ventriculophasic Reflex]]<br />
<br />
===Also read===<br />
*[[Introduction to Arrhythmias]]<br />
*[[Mechanisms of Arrhythmias]]<br />
*[[Supraventricular Rhythms]]<br />
*[[Sinus node rhythms and arrhythmias]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Clinical_Disorders&diff=5641
Clinical Disorders
2007-12-26T05:24:14Z
<p>195.229.242.57: vic4tc4tal</p>
<hr />
<div>acvarlilas<br />
c4tletoca<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor=<br />
}}<br />
<br />
==Medication==<br />
===Digoxin===<br />
[[Image:med_digitalis.png|thumb|Typical for digoxin intoxication is the odd shaped ST-depression]]<br />
ECG changes typical for digoxin intoxication (digoxin = Lanoxin) are:<br />
*odd shaped ST-depression. <br />
*T-wave flat, negative or biphasic<br />
*Short QT interval<br />
*Increased u-wave amplitude<br />
*Prolonged PR-interval<br />
*Brady-arrhytmias:<br />
**Sinusbradycardia<br />
**AV block. Including complete AV block and Wenkebach.<br />
*Tachyarrhythmias:<br />
**Junctional tachycardia<br />
**Atrialtachycardia<br />
**Ventricular ectopia, bigemini, monomorphic ventricular tachycardia, bidirectional ventricular tachycardia<br />
<br />
Intoxication can lead to a SA-block or AV-block, sometimes in combination with a tachycardia. '''NB''' these effects are increased by hypokaliemia. In extreme high concentrations rhythmdisturbances (''ventricular tachycardia, ventricular fibrillation, atrial fibrillation'') may develop.<br />
<br />
===Anti-arhythmics===<br />
* '''anti-arhythmics:''' These may lead to several ECG-changes;<br />
**broad and irregulair P-wave<br />
**broad QRS-complex<br />
**prolonged QT-interval (brady-, tachycardia, AV-block, ventricular tachycardia)<br />
**prominent U-wave<br />
**In case of intoxication, the above mentioned characteristics are more prominent<br />
<br />
Additionally, several arrhtythmias can be seen.<br />
<br />
=== Nortriptyline intoxication ===<br />
[[Image:ECG_nortr_intox.png|thumb| An example of severe nortriptyline intoxication. The inhibitory effect of the sodiumchannel manifests as a broadened QRS complex and a prolonged QT interval.]]<br />
[[Image:ECG_TCA_intox.jpg|thumb| Another example of severe nortriptyline intoxication.]]<br />
{{clr}}<br />
<br />
=== Amitriptyline intoxication ===<br />
[[Image:ECG_amitr_OD_during.jpg|thumb| An example of a severe amitriptylin intoxication. The inhibitory effect of the sodiumchannel manifests as a broadened QRS complex.]]<br />
[[Image:ECG_amitr_OD_before.jpg|thumb| An ECG of the same patient before the intoxication.]]<br />
<br />
{{clr}}<br />
<br />
==Pericarditis==<br />
[[Pericarditis]]<br />
<br />
==Myocarditis==<br />
<br />
[[w:Myocarditis|Myocarditis]] is an inflammation of the myocardium and the interstitium. The symptoms are faint chestpain, abnormal heartrate and progressive heartfailure. It can be caused by several factors: viral, bacterial, fungi, parasites, spirochaet, auto-immune, borreliosis (Lyme's disease) and HIV/AIDS. <br />
<br />
Acute peri/myocarditis causes aspecific ST changes. These can be accompanied with supraventricular and ventricular rhythmdisturbances and T-wave abnormalities.<br />
<br />
==Pulmonary embolism==<br />
See the chapter [[Pulmonary Embolism]]<br />
<br />
==Chronic pulmonary disease pattern==<br />
The ECG shows low voltaged QRS-complexes in leads I, II, and III and a right axisdeviation. This is caused by the increased pressure on the right chamber. This leads to right ventricular hypertrophy.<br />
<br />
==Pacemaker==<br />
See the chapter [[Pacemaker]]<br />
<br />
==Tamponade==<br />
[[Image:PulsusAlternans.jpg|thumb]]<br />
In case of a tamponade, fluid collects in the pericardium. As the pericardium is stiff, the heart is compressed resulting in relaxation, and thus, filling difficulties. This is a potential life-threatening situation and should be treated with pericardiocenteses, which is drainage of the fluid. Tamponade can be the results of pericarditis or myocarditis. Also, after a myocardial infarction a tamponade may develop, this is called Dresslers' Syndrome. In case of cancer, pericardial fluid may develop. This is usually caused by a Pericarditis carcinomatosa, meaning that the cancer has spread to the pericardium<br />
<br />
The ECG shows:<br />
*Sinus tachycardia<br />
*Low-voltaged QRS complexes [[microvoltages]]<br />
*Alternation of the QRS complexes, usually in a 2:1 ratio. Electrical alternans can also be seen in myocardial ischemia, acute pulmonary embolism, and tachyarrhythmias<br />
*PR segment depression (this can also be observed in an [[Ischemia#Atriaal_.2F_boezem_infarct|atrial infarction]])<br />
{{clr}}<br />
<br />
==Ventricular Aneurysm==<br />
The ECG pattern suggests an acute MI. All classical signs of MI may occur:; Q-waves, ST-elevations (>1mm, >4 weeks present)and T-wave inversions are present. To exclude an acute MI, comparison with old ECG's is compulsory (MI has occurred years before).<br />
<br />
==Dilated Cardiomyopathy==<br />
Often, a LBBB or broadened QRS-complex can be seen. Additionally, aspecific ST changes are present with signs of left atrial enlargement.<br />
<br />
==Hypertrophic Obstructive Cardiomyopathy==<br />
A HOCM is an heditary illness.<br />
On the ECG there are signs of [[hypertrophy|left ventricular hypertrophy]] and [[P wave morphology|left atrial enlargement]].<br />
<br />
==Electrolyte disturbances==<br />
See chapter: [[electrolyte disturbances]]<br />
<br />
==Hypothermia==<br />
In hypothermia a number of specific changes can be seen;<cite>hypoth</cite><br />
* sinubradycardia<br />
* prolonged QTc-interval<br />
* ST-elevation (inferior and left precordial leads)<br />
* Osborne-waves (slow deflexions at the end of the QRS-complex)<br />
<br />
[[Image:osborne.gif|thumb| An Osborne J wave]]<br />
{{clr}}<br />
<br />
==ECG changes after neurologic events==<br />
[[Image:ECG_SAB.png|thumb| ECG of a 74 year old patient with a subarachnoid hemorrhage. Note the negative T-waves and the prolonged QT interval.]]<br />
In 1938, Aschenbrenner <cite>Aschenbrenner</cite> noted that repolarisation abnormalities may occur after increased intracranial pressure. Since then, many publications have occurred discribing ECG changes after acute neurological events.<br />
<br />
De ECG changes that may occur are: <br />
*q-waves<br />
*ST-elevations, <br />
*ST-depressions, <br />
*T-wave changes. Large negative T waves over the precordial leads are observed frequently.<br />
*prolonged QT-interval.<br />
*prominent u-waves.<br />
<br />
These abnormalites are frequently seen after [[w:Subarachnoid_hemorrhage|subarachnoid_hemorrhage (SAH)]] (if measured serially, almost every SAH patients has at least one abnormal ECG.), but also in [[w:Subdural_haematoma|subdural haematoma]], ischemic [[w:Cerebrovascular_accident|CVA]]'s, [[w:Brain_tumor|brain Tumors]], [[w:Guillain-Barre|Guillain Barré]], [[w:Epilepsy|epilepsy]] and [[w:Migraine|migraine]]. The ECG changes are generally reversible and have linited prognostic value. However, the ECG changes can be accompanied with myocardial damage and echocardiographic changes. The cause of the ECG changes is not yet cl;ear. The most common hypothesis is that of a neurotramittor "catecholaminestorm" caused by sympathtic stimulation.<br />
<br />
==Cardiac contusion==<br />
Cardiac contusion (in latin: contusio cordis or commotio cordis) is caused by a blunt trauma to the chest, often caused by a car- or motorbikeaccident or in martial arts<cite>Maron</cite>. Rhythmdisturbances may occur and even heartfailure. Diagnosis is made using echocardiography and laboratorytesting for cardiac enzymes. <br />
Possible ECG changes are:<cite>Sybrandy</cite><br />
<br />
'''Not-specific changes'''<br />
*Pericarditis-like ST elevation or PTa depression<br />
*Prolonged QT interval<br />
'''Myocardial damage'''<br />
*New Q waves<br />
*ST-T segment elevation or depression<br />
'''Conduction delay'''<br />
*Right bundelbranchblok<br />
*Fascicular blok<br />
*AV delay(1st, 2nd, and 3rd degree AV blok)<br />
'''Arrhythmias'''<br />
*Sinustachycardia<br />
*Atrial and ventricular extrasystoles<br />
*Atrial fibrillation<br />
*Ventricular tachycardia<br />
*[[Arrhythmias#Ventricular fibrillation|Ventricular fibrillation]]<br />
*Sinusbradycardia<br />
*Atriala tachycardia<br />
<br />
==Lown Ganong Levine Syndrome==<br />
The Lown Ganong Levine Syndrome is a pre-excitation syndrome in which the atria are connected to the lower part of the AV node or bundle of His. On the ECG:<br />
* short PR interval, < 120 ms<br />
* normal QRS complex<br />
* no delta wave<br />
==Left and right bundelbranch block==<br />
See: [[Conduction_delay|Conduction delay]]<br />
<br />
==References==<br />
<biblio><br />
#Sybrandy pmid=12695446<br />
#Rodger pmid=11018210<br />
#Ferrari pmid=9118684<br />
#Aschenbrenner Aschenbrenner R, Bodechtel G, ''ÃÂber Ekg.-Veränderungen bei Hirntumorkranken''. Journal of Molecular Medicine, 17, 9, 2/1/1938, Pages 298-302, http://dx.doi.org/10.1007/BF01778563<br />
#Maron pmid=14681516<br />
#hypoth pmid=2738372<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Ventricular_Arrhythmias&diff=5640
Ventricular Arrhythmias
2007-12-26T05:23:49Z
<p>195.229.242.57: licotatrrict</p>
<hr />
<div>zeloude<br />
basdel<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
'''Tachycardias:'''<br />
*[[Ventricular Tachycardia]]<br />
*[[Ventricular Flutter]]<br />
*[[Ventricular Fibrillation]]<br />
*[[Torsade de Pointes]]<br />
*[[Bundle-branch re-entrant tachycardia]]<br />
*[[Idioventricular Rhythm]]<br />
*[[Accelerated Idioventricular Rhythm]]<br />
<br />
'''[[Ectopic Beats]]''':<br />
*[[Ventricular Premature Beats]]<br />
<br />
<br />
<br />
'''Also read:'''<br />
*Flowchart: [[media:wideQRS_tachycardia_flow.png|Approach to the Wide Complex Tachycardia]]<br />
*[[Introduction to Arrhythmias]]<br />
*[[Mechanisms of Arrhythmias]]<br />
*[[Supraventricular Rhythms]]<br />
*[[Junctional Tachycardias]]<br />
*[[Sinus node rhythms and arrhythmias]]<br />
*[[Ventriculophasic Reflex]]<br />
<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''An overview of ventricular tachycardias''', follow the [[media:wideQRS_tachycardia_flow.png|wide complex tachycardia flowchart]]<br />
|-<br />
!<br />
!regularity<br />
!atrial frequency<br />
!ventricular frequency<br />
!origin (SVT/VT)<br />
!p-wave<br />
!effect of adenosine<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Wide complex (QRS>0.12)'''<br />
|-<br />
! [[Ventricular Tachycardia]]<br />
| regular (mostly)<br />
| 60-100 bpm<br />
| 110-250 bpm<br />
| ventricle (VT)<br />
| AV-dissociation<br />
| no rate reduction (sometimes accelerates)<br />
|-<br />
! [[Ventricular Fibrillation]]<br />
| irregular<br />
| 60-100 bpm<br />
| 400-600 bpm<br />
| ventricle (VT)<br />
| AV-dissociation<br />
| none<br />
|-<br />
! [[Ventricular Flutter]]<br />
| regular<br />
| 60-100 bpm<br />
| 150-300 bpm<br />
| ventricle (VT)<br />
| AV-dissociation<br />
| none<br />
|-<br />
! [[Accelerated Idioventricular Rhythm]]<br />
| regular (mostly)<br />
| 60-100 bpm<br />
| 50-110 bpm<br />
| ventricle (VT)<br />
| AV-dissociation<br />
| no rate reduction (sometimes accelerates)<br />
|-<br />
! [[Torsade de Pointes]]<br />
| regular<br />
| <br />
| 150-300 bpm<br />
| ventricle (VT)<br />
| AV-dissociation<br />
| no rate reduction (sometimes accelerates)<br />
|-<br />
|}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Normal_Tracing&diff=5639
Normal Tracing
2007-12-26T05:23:23Z
<p>195.229.242.57: rololocn</p>
<hr />
<div>trocricpasac<br />
domdarnod<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor= <br />
}}<br />
'''Characteristics of a normal ECG:'''<br />
* [[Rhythm]]: [[Sinus node rhythms and arrhythmias|sinus rhythm]]<br />
* [[Rate]]: 60-100 bpm<br />
* [[Conduction]]:<br />
** [[Conduction#The PQ interval|PQ interval]] 120-200ms<br />
** [[Conduction#The QRS interval|QRS width]] 60-100ms<br />
** [[Conduction#The QT interval|QTc interval]] 390-450ms (use the [[QTc calculator]] for this)<br />
* [[Heart axis]]: between -30 and +90 degrees<br />
* [[P wave morphology]]: <br />
** The maximal height of the P wave is 2.5 mm in leads II and / or III<br />
** The p wave is positive in II and AVF, and bifasic in V1<br />
** The p wave duration is usually shorter than 0.12 seconds<br />
* [[QRS morphology]]:<br />
**No [[Q waves|pathological Q waves]]<br />
**No left or right ventricular [[hypertrophy]]<br />
**No [[microvoltations]]<br />
**Normal R wave propagation. (R waves increase in amplitude from V1-V5)<br />
* [[ST morphology]]<br />
**No [[ST morphology|ST elevation or depression]]<br />
**T waves should be [[ST morphology|concordant with the QRS complex]]<br />
<br />
* The ECG should not have changed from the previous ECG</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Genetic_Arrhythmias&diff=5638
Genetic Arrhythmias
2007-12-26T05:23:10Z
<p>195.229.242.57: tac4tgetlili</p>
<hr />
<div>cgetdomzel<br />
zelzelc<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
*[[Long QT Syndrome]]<br />
*[[Brugada Syndrome]]<br />
*[[Arrythmogenic Right Ventricular Cardiomyopathy]]<br />
*[[Catecholamin Induced Ventricular Tachycardia]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=P_Wave_Morphology&diff=5637
P Wave Morphology
2007-12-26T05:22:54Z
<p>195.229.242.57: domrol</p>
<hr />
<div>tapasta<br />
liacc4tchi<br />
{{nav|<br />
|previouspage=Heart axis<br />
|previousname=Step 4:Heart axis<br />
|nextpage=QRS morphology<br />
|nextname=Step 6: QRS morphology<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= A. Bouhiouf, Msc<br />
}}<br />
<br />
The ''p wave morphology'' can reveal right or left atrial stretch.<br />
<br />
The P-wave morphology is best determined in leads II and V1 during sinus rhythm.<br />
<br />
===The normal P wave===<br />
[[Image:normalSR.jpg|thumb|Normal sinus rhythm with a positive p wave in leads I, II en AVF and a biphasic p wave in V1.]]<br />
Characteristics of a normal p wave:<cite>Spodick</cite><br />
*The maximal height of the P wave is 2.5 mm in leads II and / or III<br />
*The p wave is positive in II and AVF, and bifasic in V1<br />
*The p wave duration is usually shorter than 0.12 seconds<br />
<br />
Elevation or depression of the [[PTa segment]] (the part between the p wave and the beginning of the QRS complex) can result from [[Ischemia#Atrial infarction|Atrial infarction]] or [[Clinical Disorders#Pericarditis|pericarditis]].<br />
<br />
If the p-wave is enlarged, the [[Chamber_Hypertrophy_and_Enlargment#Left_atrial_enlargement|atria are enlarged]].<br />
{{clr}}<br />
<br />
<br />
==Referenties==<br />
<biblio><br />
#Spodick pmid=1575201<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=ECGpedia:Help&diff=5636
ECGpedia:Help
2007-12-26T05:22:34Z
<p>195.229.242.57: baschimo</p>
<hr />
<div>norotrroo<br />
ouboacelt</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Conduction&diff=5635
Conduction
2007-12-26T05:22:20Z
<p>195.229.242.57: bocchic</p>
<hr />
<div>c4tdelcnale<br />
acelerr<br />
{{nav|<br />
|previouspage=Rate<br />
|previousname=Step 2: Rate<br />
|nextpage=Heart axis<br />
|nextname=Step 4: Learn how to determine the heart axis<br />
}}<br />
<br />
[[Image:QRSwaves.jpg|thumb]]<br />
==The PQ interval==<br />
The PQ interval starts at the beginning of the atrial contraction and ends at the beginning of the ventricular contraction.<br />
[[Image:PR_interval_buildup.svg|thumb|The PR duration depends on the conduction velocity in the atria, AV node, His bundle, bundle branches and Purkinje fibers.]]<br />
<br />
<br />
The PQ interval (sometimes referred to as the PR interval as a Q wave is not always present) indicates how fast the action potential is transmitted through the AV node (atrioventricular) from the atria to the ventricles. Measurement should start at the beginning of the P wave to the beginning of the QRS segment.<br />
<br />
'''The normal PQ interval is between 0.12 and 0.20 seconds'''.<br />
<br />
A prolonged PQ interval is a sign of a degradation of the conduction system, increased vagal tone (Bezold-Jarisch reflex), or it can be pharmacologically induced. <br />
<br />
This is called [[Arrhythmias#Atrioventricular_block|1st, 2nd or 3rd degree AV block]].<br />
<br />
A short PQ interval can be seen in the [[Arrhythmias#WPW_syndrome|WPW syndrome]] in which a faster connection exists between the atria and the ventricles.<br />
{{clr}}<br />
<br />
==The QRS duration==<br />
The QRS duration indicates how fast the ventricles depolarize. <br />
<br />
The ventricles depolarize normally within 0.10 seconds. When this is longer than 0.12 seconds, this is a [[conduction delay| conduction delay]]. Possible causes of a QRS duration > 0.12 seconds include:<br />
* [[LBBB|Left bundle branch block]]<br />
* [[RBBB|Right bundle branch block]]<br />
* [[Electrolyte Disorders]]<br />
* [[Idioventricular Rhythm|Idioventricular rhythm]] and [[Pacemaker|paced rhythm]]<br />
<br />
==The QT interval==<br />
The QT interval indicates how fast the ventricles are repolarized and how fast they are ready for a new heart cycle<br />
The normal value for QTc(orrected) is: 440-450ms for men and 450-470ms for women. <cite>Moss</cite><br />
<br />
[[Image:QRSinterval.jpg|thumb| The QT interval start at the onset of the Q wave and ends where the tangent line for the steepest part of the T wave intersects with the baseline of the ECG. Click on the image for a bigger image]]<br />
<br />
The QT interval comprises the QRS-complex, the ST-segment, and the T-wave.<br />
<br />
In a (serious) prolonged QT time, is takes longer for the myocardial cells to be ready for a new cardiac cycle. There is a possibility that some cells are not yet repolarized, but that a new cardiac cycle is already initiated. These cells are at risk for uncontrolled depolarization and induce a [[Arrhythmias#Torsade_de_pointes|torsade de pointes]], a ventricular tachycardia.<br />
<br />
The QT interval is defined as follows: <cite>Lepeschkin</cite> The time between the beginning of the Q until the point where the steepest tangent line from the end of the T-wave intersects with the base line of the ECG. <br />
<br />
The difficult part is that the QT interval gets shorter if the heart rate increases. This cab be solved by correcting the QT time for heart rate using the Bazett formula::<br />
<br />
[[Image:Formule_QTc.png]]<br />
<br />
''at an RR interval 1 second, the (heart frequency 60/min) QTc=QT''<br />
<br />
Using the QTc calculator on the right, the QTc is easy extractable.<br />
<br />
<flash>file=QTc.swf|width=300|height=200|quality=best|align=right|salign=R||bgcolor=#FFF5F5</flash><br />
<br />
On the modern ECG machines, the QTc is given. However, the machines are not always capable of recognizing the correct QT time. Therefore, it is important to check this manually..<br />
<br />
The following formula is indicative for normal values of QT time (uncorrected):<br />
<br />
[[Image:Formule_QTn_nl.png]]<br />
{{clr}}<br />
<br />
===Difficult QT intervals===<br />
In some examples of the QT interval it can be difficult to measure a correct QT time. We have made a separate chapter: [[Difficult_QT| Measurement of difficult QT intervals]].<br />
<br />
===Causes of a prolonged QT interval===<br />
*Medication (i.e. anti-arrhythmics, tricyclic antidepressants, phenothiazedes, for a complete list look on [http://www.torsades.org Torsades.org]<br />
*Inherited [[Long QT syndrome|long QT syndrome]] (LQTS)<br />
*Cerebral (subarachnoid haemorrhage, stroke, trauma)<br />
*Post infarct<br />
<br />
===Short QT syndrome===<br />
If QTc is < 340ms [[Short_QT_Syndrome|short QT syndrome]] can be considered.<br />
<br />
== References ==<br />
<biblio><br />
#bazett Bazett HC. ''An analysis of the time-relations of electrocardiograms''. Heart 1920;7:353-370.<br />
#Lepeschkin pmid=14954534<br />
#Gaita pmid=12925462<br />
#Moss pmid=8256751<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Intraventricular_Conduction&diff=5634
Intraventricular Conduction
2007-12-26T05:22:00Z
<p>195.229.242.57: pasbocouli</p>
<hr />
<div>chicnalet<br />
elroldarge<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[T.T. Keller]]<br />
|Supervisor=<br />
}}<br />
==Conduction delay==<br />
[[Image:geleidingssysteem.jpg|thumb| If the conduction system is dysfunctional, the QRS widens beyond 0.12 seconds.]]<br />
If the QRS complex is wider than 0.12 seconds this is mostly caused by a delay in the conduction tissue of one of the bundle branches:<br />
*[[#LBBB| Left Bundle Branch Block (LBBB))]]<br />
*[[#RBBB| Right Bundle Branch Block(RBBB)]]<br />
*Interventricular conduction delay<br />
A right or left axis rotation can be caused by a:<br />
*[[#Criteria for LAFB| left anterior fascicular block (LAFB)]]<br />
*[[#Criteria for LPFB| left posterior fascicular block (LPFB)]]<br />
<br />
Sometimes this conduction delay is '''frequency-dependent ''': the bundle branch block occurs only at higher heart rates and disappears at slower heart rates.<br />
{{clr}}<br />
<br />
== LBBB vs RBBB ==<br />
[[Image:Verschil_LBTB-RBTB.png|thumb| A bundle branch block causes a delay in the depolarization of the right (RBBB) or left (LBBB) ventricle. In RBBB the QRS complex shows a second peak or R' in V1.]]<br />
Check V1 when QRS > 0,12 sec.<br />
When the last QRS in V1 is below the baseline (moving away from V1), a LBBB is the most likely diagnosis. <br />
When the last activity is above the baseline, it's a RBBB.<br />
If the QRS > 0.12 sec. but the morphological criteria of LBBB or RBBB do not apply, it is called 'interventriculair conduction delay', a general term. <br />
{{clr}}<br />
<br />
==Left Bundle Branch Block (LBBB)==<br />
{{:LBBB}}<br />
<br />
==Right Bundle Branch Block (RBBB)==<br />
{{:RBBB}}<br />
<br />
==Left Anterior Fascicular Block (LAFB)==<br />
[[Image:LAHB.png|thumb| Left anterior hemiblock]]<br />
;Criteria for left anterior fascicular block<br />
:left axis deviation (<-30ð)<br />
:no or very small S in lead I<br />
:normal small q in lead I<br />
:S > R in leads II and III<br />
:no or very few QRS widening<br />
In ''left anterior fascicular block'' the anterior part (fascicle) of the left bundle is slow. This results in delayed depolarisation of the upper anterior part of the left ventricle. On the ECG this results in left axis deviation. The QRS width is <0,12 seconds in isolated LAFB.<br />
{{clr}}<br />
<br />
==Left Posterior Fasicular Block (LPFB)==<br />
;Criteria for posterior fascicular block:<br />
:right [[heart axis|axis devation]] >+120ð; <br />
:deep S in I; <br />
:small q in III; <br />
:no or very few QRS widening;<br />
:Right ventricular [[hypertrophy]] and previous [[Ischemia#Lateral|lateral myocardial infarction]] have been excluded<br />
<br />
==Mechanisms of aberrant conduction==<br />
;Aberrant ventricular conduction is defined as<br />
:QRS widening due to delay or block in bundle branch or intramyocardial conduction<cite>wellens</cite><br />
Aberrancy can result from:<br />
#A sudden fastening of the heart rate that the bundles cannot conduct (phase 3 aberration)<br />
#Retrograde concealed conduction<br />
#A slow heart rate (phase 4 aberration)<br />
<br />
Right bundle branch block is most common, because the right bundle has the longest refractory period. Left bundle branch block accounts for about 1/3rd of cases.<br />
<br />
===Phase 3 Aberration===<br />
Phase 3 aberration occurs when conduction fibers receive a new impulse, before they have fully repolarized. This can sometimes be observed at the start of paroxysmal supraventricular tachycardias or in a long-short sequence where the refractory periode of the long sequence is prolonged.<br />
===Retrograde Concealed Conduction===<br />
Phase 3 aberration is often the cause of the first wide QRS complex. However at a regular rate retrograde concealed conduction is often the sustaining mechanism. The sequence of QRS widening that is often observed is phase 3 aberration in the first premature beat. This can leave the left bundle (as an example) refractory for the next beat. This next beat is conducted by the right bundle and once it reaches the apex, it is conducted retrograde by the left bundle. This can continue until a new premature ventricular beat causes a compensatory pause and 'resets' the system.<br />
<br />
===Phase 4 Aberration===<br />
Phase 4 aberration only occurs after prolonged pause. During such a pause (e.g. in second degree AV block) the fibers of the Purkinje system can 'hyper'-depolarize spontaneously. As their membrane potential becomes more and more negative the conduction velocity reduces and they can even block altogether. This also requires an upwards shift of the threshold membrane potential and a change in membrane responsiveness, so it is rarely seen in normal hearts.<br />
<br />
==References==<br />
<biblio><br />
#Garcia isbn=0763722464<br />
#wellens isbn=9781416002598<br />
<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Myocardial_Infarction&diff=5633
Myocardial Infarction
2007-12-26T05:21:40Z
<p>195.229.242.57: aceldelact</p>
<hr />
<div>zelallet<br />
vitrocrol<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|supervisor= <br />
}}<br />
Ischemia occurs when part of the heartmuscle, the myocardium, is deprived form oxygen and nutrients. <br />
Common causes of ischemia are:<br />
* Narrowing or obstruction of a coronary artery.<br />
* A rapid arrhythmia, causing a disbalance in supply and demand of energy. <br />
<br />
A short period of ischemia causes ''reversibele'' effects: The heartcells will be able to recover. When the ep[isode of ischemia lasts for a longer period of time, heartmuscle cells will die. This is called a '''heart attack''' or '''myocardial infarction'''. That is why it is critical to recognize ischemia on the ECG in an early stage. <br />
<br />
Severe ischemia will reuslts in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment. <br />
<br />
'''Signs and symptoms of myocardial ischemia:'''<br />
* Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower jaw or the left arm<br />
* Fear of dying <br />
* Nausea<br />
* Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock <br />
* Rhythm dysturbances (in particular increasing prevalnce of ventricular ectopia, ventricular tachycardia, AV block)<br />
<br />
===Risk assessment of Cardiovascular disease===<br />
The narrowing of the coronary artery leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or stroke, can be estimated using [http://www.escardio.org/initiatives/prevention/prevention-tools/SCORE-Risk-Charts.htm SCORE system] which is developed by the European Society of cardiology (ESC). <br />
As shown in the figure, the most important risk factors for myocardial infarction are:<br />
*Male sexe<br />
*Smoking<br />
*Hypertension<br />
*Diabetes Mellitus<br />
*Hypercholesterolemia<br />
<br />
===Risk assessment of ischemia===<br />
An [[Exercise Testing|exercise test]] such as a bicycle or treadmilltest, may be usefull in detecting myocardial ischemia after exercise.<cite>accexercise</cite> In such a test, a continuous ECG registration is performed during exercise. The ST-segment, blood pressure asnd clinical status of the patient (i.e. chest complaints) are monitorered during and after the test.<br />
<br />
An [[Exercise Testing|exercise test]] is positive for myocardial ischemia when the following criteria are met: <br />
* Horizontal or downsloping ST-depression of > 1mm, 60 or 80ms after the J-point<br />
* ST elevation of > 1.0 mm<br />
{{clr}}<br />
<br />
==Diagnosis of myocardial infarction==<br />
[[Image:Stelevatie_en.png|thumb|ST elevation is measured 60ms or 80ms after the J point]]<br />
<br />
The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial infarction is defined as:<cite>Alpert</cite><br />
<br />
* Elevated blood levels of cardiac enzymes ([[w:Creatine_kinase|CKMB]] or [[w:Troponin|Troponin T]]) AND <br />
* One of the following criteria are met:<br />
** The patient has typical complaints<br />
** The ECG shows ST elevation or depression<br />
** [[Pathologic_Q_Waves|pathological Q waves]] develop on the ECG<br />
** A coronary intervention had been performed (such as stent placement)<br />
<br />
So detection of elevated serum heartenzymes is more important than ECG changes. However, the heartenzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So especially in the first few hours after the myocardial infarction the ECG can be crucial.<br />
<br />
;Significant ST elevation is defined as:<br />
:ST elevation of more than 2mm in two chest leads or more than 1 mm in two adjacent limb leads<br />
:ST elevation is measured 60ms or 80ms after the J-point<br />
<br />
A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).<cite>martin</cite><br />
<br />
Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but is explained in these seperate chapters:<br />
*[[MI Diagnosis in LBBB]]<br />
*[[MI Diagnosis in RBBB]]<br />
*[[MI Dagnosis in Paced Rhythm]]<br />
{{clr}}<br />
<br />
==The location of the infarct==<br />
[[Image:coronary_anatomy.png|thumb| An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.]]<br />
[[Image:lead_overview.png|thumb|Overview of the seperate ECG leads. The lead with ST elevation 'highlights' the infarct. An infarction of the inferior wall will result in ST elevation in leads II, III and AVF. A lateral wall infarct results in ST elevation in leads I and AVL. An Anterior wall infarct results in ST-elevation in the precordial leads.]]<br />
[[Image:MI_colours_en.png|The coloured figure shows contiguous leads in matching colours|thumb]]<br />
[[Image:MIregions.jpg|thumb|The ST elevation points at the infarct location. Inferior MI = ST elevation in red regions (lead II,III and AVF). Lateral MI = ST elevation in blue leads (lead I, AVL, V5-V6). Anterio MI: ST elevation in yellow region (V1-V4). Left main stenosis: ST elevation in gray area (AVR) ]]<br />
The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an '''anterior wall infarction''' is different than those of an '''inferior wall infarction'''. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.<br />
<br />
The heart is supplied of oxygen and nutrients by the right and left coronary arteries. The left coronray artery (the '''Left Main''' or LM) divides itself in the '''left anterior descending''' artery (LAD) and the '''ramus circumflexus''' (RCX). The '''right coronary artery''' (RCA) connects to the ramus descendens posterior (RDP). With 20% of the normal population the RDP is supplied by the RCX. This called '''left dominance'''.<br />
<br />
Below you can find several different types of myocardial infarcation. Click on the specific infarct location to see examples.<br />
<br />
<br />
{| class="wikitable"<br />
|- <br />
|+'''Help with the localisation of a myocardial infarct'''<br />
|-<br />
!localisation<br />
!ST elevation<br />
!Reciproke ST depression<br />
!coronary artery<br />
|-<br />
| [[Anterior MI]] <br />
| V1-V6<br />
| None<br />
| LAD<br />
|-<br />
| [[Septal MI]]<br />
| V1-V4, disappearance of septum Q in leads V5,V6<br />
| none<br />
| LAD<br />
|-<br />
| [[Lateral MI]]<br />
| I, aVL, V5, V6<br />
| II,III, aVF<br />
| RCX or MO<br />
|-<br />
| [[Inferior MI]]<br />
| II, III, aVF<br />
| I, aVL<br />
| RCA (80%) or RCX (20%)<br />
|-<br />
| [[Posterior MI]]<br />
| V7, V8, V9<br />
| high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view)<br />
| RCX<br />
|-<br />
| [[Right Ventricle MI]]<br />
| V1, V4R<br />
| I, aVL<br />
| RCA<br />
|-<br />
| [[Atrial MI]]<br />
| PTa in I,V5,V6<br />
| PTa in I,II, or III<br />
| RCA<br />
|-<br />
|}<br />
{{clr}}<br />
<br />
The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report, the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.<cite>AHACAG</cite><br />
<br />
==Development of the ECG during persistent ischemia==<br />
[[Image:AMI_evolutie.png|thumb| The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave]]<br />
[[Image:PathoQ.png|thumb| A [[Pathologic_Q_Waves|pathological Q wave]]]]<br />
[[Image:anteriorMInegativeT.png|thumb| Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated.<cite>Novotny</cite><cite>Jensen</cite><cite>Chevalier</cite>]]<br />
The cardiomyocytes in the ''subendocardial'' layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction ''transmural ischemia'' develops. <br />
<br />
In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, '''large peaked T waves''' (or ''hyperacute'' T waves), then '''ST elevation''', then'''negative T waves''' and finally '''[[Pathologic_Q_Waves|pathologic Q waves]]''' develop.<br />
<br />
{| class="wikitable"<br />
|- <br />
|+'''Evolution of the ECG during a myocardial infarct'''<br />
|-<br />
!<br />
!see figure<br />
!change<br />
|-<br />
!minutes<br />
| not in figure<br />
b<br />
| hyperacute T waves (peaked T waves)<br />
ST-elevation<br />
|-<br />
!hours<br />
| c<br />
d<br />
| ST-elevation, with terminal negative T wave<br />
negative T wave (these can last for months)<br />
|-<br />
!days<br />
| e<br />
| [[Pathologic_Q_Waves|Pathologic Q Waves]]<br />
|-<br />
|}<br />
<br />
{{clr}}<br />
<br />
==References==<br />
<biblio><br />
#Wung pmid=16777513<br />
#martin pmid=17825710<br />
#Alpert pmid=10987628<br />
#accexercise pmid=12356646 <br />
#Menown pmid=10653675<br />
#LBTB pmid=11265742<br />
#AHACAG pmid=1116248<br />
#Novotny pmid=18019666<br />
#Chevalier pmid=12716101<br />
#Jensen pmid=15851335<br />
</biblio><br />
<br />
==External Links==<br />
A good introduction to [http://www.askdrwiki.com/mediawiki/index.php?title=Coronary_Angiography coronary angiography]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=AV_Conduction&diff=5632
AV Conduction
2007-12-26T05:21:11Z
<p>195.229.242.57: acelnotr</p>
<hr />
<div>lirolacl<br />
varall<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt]]<br />
|supervisor= <br />
}}<br />
[[Image:AV_block_sequence.png|thumb|Sequence of AV block from incomplete to complete]]<br />
Conduction disturbances can occur at the level of the sinoatrial (SA) node, the atrioventricular (AV) node and the bundle branch system. <br />
In atrioventricular block the conduction between atria and ventricles is disturbed leading to an incread [[Conduction#PQ interval|PQ interval]] or to drop out of QRS complexes: atrial activity that is not followed by ventricular activity. Three degrees of block can be distinguished.<br />
<br />
==First degree AV block==<br />
[[Image:Rhythm_1stAVblock.png|thumb| 1st degree AV block. Although the PQ interval is prolonged all p-waves are followed by QRS complexes: there is no dropout of beats]]<br />
In first degree AV block there is a prolongation of PQ duration (PQ time > 0.20 sec). Still every p-wave is being followed by a QRS complex.<br />
First degree AV block is present in 16% of >90-year olds <cite>kelley</cite> and is mostly caused by a degeneration of the conduction system. First degree AV block is relatively harmless.<br />
{{clr}}<br />
==Second degree AV block==<br />
In second degree AV block not all p-waves are being followed by QRS complexes: beat dropout occurs. Second degree AV block can be categorized in 3 types:<br />
===Second degree AV block type I (Wenckebach)===<br />
[[Image:Wenckebach.png|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
[[Image:Wenckebach2.png|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
[[Image:Wenckebach3.jpg|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
In second degree AV block type I, the PQ interval prolongs from beat to beat up until the drop-out of one QRS complex. The characteristics of a Wenkebach block:<br />
* QRS complexes cluster (e.g. a 5:4 block or 4:3 block)<br />
* The PQ interval prolongs every consecutive beat<br />
* The PQ interval that follows upon a dropped beat is the shortes.<br />
* The RR interval shortens (!) every consecutive beat.<br />
* The amount of block decreases during exercise (e.g. a 4:3 block improves into a 6:5 block)<br />
The conduction disturbance in a type I block originates in the AV node. Isolated second degree AV block type I is relatively benign and not a pacemaker indication.<br />
{{clr}}<br />
<br />
===Second degree AV block type II (Mobitz)===<br />
[[Image:Rhythm_Mobitz.png|thumb| Second degree AV block type II (Mobitz)]]<br />
In second degree AV block type II, beats are dropped irregularly without PQ interval prolongation. As the drop out of beats is irregular, no clustering of QRS complexes can be seen as in second degree block type I. Second degree AV block type II marks the starting of trouble and is a class I pacemaker indication. <cite>CITATION</cite><br />
The cause of second degree AV block type II can be found distally from the AV node: in the HIS bundle or in the bundle branches or Purkinje fibers. <br />
<br />
An important differential diagnosis of second degree AV block type II is an [[Atrial Premature Complexes|premature atrial complex]] with compensatory pause. This diagnosis is much more common and harmless.<br />
{{clr}}<br />
<br />
===High grade AV block===<br />
High grade AV block is defined as two or more p-waves not followed by QRS complexes.<br />
<br />
==Third degree AV block==<br />
[[Image:Rhythm_3rdAVblock.png|thumb| 3rd degree AV block. AV dissociation is present: there is no relation between p-waves and the (nodal) QRS complexes.]]<br />
[[Image:Rhythm_totalAVblock.png|thumb| Short lasting total AV block (initiated by adenosine infusion). P-waves are present, but no QRS complexes follow]]<br />
Third degree AV block is synonymous to ''total block'': absence of atrioventricular conduction. The P-waves and QRS complexes have no temporal relationship, which is called to [[AV dissociation]].<br />
The ventricular rhythm can be [[Nodal Rhythm|nodal]], [[Idioventricular Rhythm|idioventricular]] or absent. Absent ventricular rhythm results in asystole and death.<br />
<br />
During third degree AV block the blood supply to the brain can insufficient, leading to loss of consciousness. [[w:Stokes-Adams_Attack|Adams Stokes (or Stokes-Adams) attacks]] (often misspelled as Adam Stokes) attacks arte attacks of syncope or pre-syncope in the setting of third degree AV block.<br />
{{clr}}<br />
==References==<br />
<biblio><br />
#kelley pmid=17126661<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Repolarization_(ST-T,U)_Abnormalities&diff=5631
Repolarization (ST-T,U) Abnormalities
2007-12-26T05:20:29Z
<p>195.229.242.57: lizele</p>
<hr />
<div>sitbomonouge<br />
cnacacpasre<br />
{{ActiveDiscuss}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt]]<br />
|moderator= [[user:VdBilt|I.A.C. van der Bilt]]<br />
|supervisor=<br />
}}<br />
*[[Repolarization (ST-T,U) Abnormalities|Early repolarization (normal variant)]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Juvenile T waves (normal variant)]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Nonspecific abnormality, ST segment and/or T wave]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST and/or T wave suggests ischemia]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST suggests injury]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST suggests ventricular aneurysm]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Q-T interval prolonged]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Prominent U waves]]<br />
*[[Cardiac Memory|Cardiac Memory]]*</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Sinus_Node_Rhythms_and_Arrhythmias&diff=5630
Sinus Node Rhythms and Arrhythmias
2007-12-26T05:19:56Z
<p>195.229.242.57: cnarac</p>
<hr />
<div>eltbasra<br />
chielt<br />
trdelpas<br />
{{nav|<br />
|previouspage=Basics<br />
|previousname=Basics<br />
|nextpage=Rate<br />
|nextname=Step 2: Heart Rate<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user: Vdbilt|I.A.C. van der Bilt]]<br />
|supervisor= <br />
}}<br />
==Normal heart rhythm==<br />
[[Image:conduction_system_en.png|thumb|The conduction system handles the spreading of an electrical signal through the heart. The normal sinus rhythm begins in the sinus node and goes via the AV node to the His bundle where it splits via the right and left bundle branch.]]<br />
[[Image:PQRS_origin_en.png|thumb| During normal sinus rhythm, every atrial contraction (P-wave) is followed by a ventricular contraction (QRS complex).]]<br />
[[Image:normalSR.jpg|thumb|Normal sinus rhythm with a positive P-wave in I, II and AVF, and a biphasic P-wave in V1.]]<br />
The normal heart rhythm is ''sinus rhythm''. That means that the rhythm has its origin in the sinus node, the heart's fastest physiological impulse generator.<br />
The sinus node (SA) is located in the upper part of the wall of the right atrium. When the sinus node generates an electrical impulse, first the cells of the right atrium depolarise, then the cells of the left atrium, the AV (atrioventricular) node follows and at last the ventricles are stimulated via the His bundle.<br />
<br />
With this knowledge it is quite simple to recognise normal sinus rhythm on the ECG.<br />
<br />
;Criteria for normal sinus rhythm (see also [[Basics]]):<br />
*A P wave (atrial contraction) precedes every QRS complex<br />
*The rhythm is regular, but varies slightly while breathing<br />
*The frequency ranges between 60 and 100 beats per minute<br />
*The P waves maximum height is 2.5 mm in II and/or III<br />
*The P wave is positive in I and II, and biphasic in V1<br />
<br />
These last two definitions will be discussed in the topic [[P wave morphology]].<br />
Heart rhythms which are not sinus rhythm are [[arrhythmias]]. <br />
<br />
==Sinus arrhythmias==<br />
Some variants of sinusrhythm exist:<br />
*[[Asystole]]<br />
*[[Sinustachycardia|Sinustachycardia (>100 beats per minute)]]<br />
*[[Sinusbradycardia|Sinusbradycardia (<50 beats per minute)]]<br />
*[[Sinusarrest|Sinus arrest or pause]]<br />
*[[Sino-atrial_exit_block|Sino-atrial exit block]]<br />
*[[Sick Sinus Syndrome]]<br />
<br />
If the heart rate exceeds 100 bpm, the [[Arrhythmias#Tachyarrhythmias|tachcyardia flow chart]] should be followed.<br />
{{clr}}<br />
==Examples==<br />
[[Image:Normaal ecg.jpg|thumb| An example of normal sinus rhythm.]]<br />
[[Image:Nsr.jpg|thumb| Another example of normal sinus rhythm.]]<br />
<br />
{{clr}}<br />
[[nl:Ritme]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=ECGpedia:General_disclaimer&diff=5629
ECGpedia:General disclaimer
2007-12-26T05:19:44Z
<p>195.229.242.57: alrotr</p>
<hr />
<div>sitolocaliba<br />
virelbo<br />
:We do our best to ascertain that all information on this site is correct and up-to-date. However, given the open structure of this site, we cannot guarantee that it is. The information provided here is for educational and informational purposes only and designed primarily for use by qualified physicians and other medical professionals. In no way should it be considered as offering medical advice.</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Sinus_Node_Rhythms_and_Arrhythmias&diff=5628
Sinus Node Rhythms and Arrhythmias
2007-12-26T05:19:32Z
<p>195.229.242.57: relelttrdome</p>
<hr />
<div>chielt<br />
trdelpas<br />
{{nav|<br />
|previouspage=Basics<br />
|previousname=Basics<br />
|nextpage=Rate<br />
|nextname=Step 2: Heart Rate<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user: Vdbilt|I.A.C. van der Bilt]]<br />
|supervisor= <br />
}}<br />
==Normal heart rhythm==<br />
[[Image:conduction_system_en.png|thumb|The conduction system handles the spreading of an electrical signal through the heart. The normal sinus rhythm begins in the sinus node and goes via the AV node to the His bundle where it splits via the right and left bundle branch.]]<br />
[[Image:PQRS_origin_en.png|thumb| During normal sinus rhythm, every atrial contraction (P-wave) is followed by a ventricular contraction (QRS complex).]]<br />
[[Image:normalSR.jpg|thumb|Normal sinus rhythm with a positive P-wave in I, II and AVF, and a biphasic P-wave in V1.]]<br />
The normal heart rhythm is ''sinus rhythm''. That means that the rhythm has its origin in the sinus node, the heart's fastest physiological impulse generator.<br />
The sinus node (SA) is located in the upper part of the wall of the right atrium. When the sinus node generates an electrical impulse, first the cells of the right atrium depolarise, then the cells of the left atrium, the AV (atrioventricular) node follows and at last the ventricles are stimulated via the His bundle.<br />
<br />
With this knowledge it is quite simple to recognise normal sinus rhythm on the ECG.<br />
<br />
;Criteria for normal sinus rhythm (see also [[Basics]]):<br />
*A P wave (atrial contraction) precedes every QRS complex<br />
*The rhythm is regular, but varies slightly while breathing<br />
*The frequency ranges between 60 and 100 beats per minute<br />
*The P waves maximum height is 2.5 mm in II and/or III<br />
*The P wave is positive in I and II, and biphasic in V1<br />
<br />
These last two definitions will be discussed in the topic [[P wave morphology]].<br />
Heart rhythms which are not sinus rhythm are [[arrhythmias]]. <br />
<br />
==Sinus arrhythmias==<br />
Some variants of sinusrhythm exist:<br />
*[[Asystole]]<br />
*[[Sinustachycardia|Sinustachycardia (>100 beats per minute)]]<br />
*[[Sinusbradycardia|Sinusbradycardia (<50 beats per minute)]]<br />
*[[Sinusarrest|Sinus arrest or pause]]<br />
*[[Sino-atrial_exit_block|Sino-atrial exit block]]<br />
*[[Sick Sinus Syndrome]]<br />
<br />
If the heart rate exceeds 100 bpm, the [[Arrhythmias#Tachyarrhythmias|tachcyardia flow chart]] should be followed.<br />
{{clr}}<br />
==Examples==<br />
[[Image:Normaal ecg.jpg|thumb| An example of normal sinus rhythm.]]<br />
[[Image:Nsr.jpg|thumb| Another example of normal sinus rhythm.]]<br />
<br />
{{clr}}<br />
[[nl:Ritme]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Frequently_Asked_Questions&diff=5626
Frequently Asked Questions
2007-12-26T05:18:59Z
<p>195.229.242.57: raczelcn</p>
<hr />
<div>ricorc<br />
sitact<br />
;Can I use a certain image / animation / video / piece of text in a non-commercial presentation?<br />
:Yes, in most cases you can. There are however certain exceptions to this rule. Some images on ECGpedia were provided by book or journal publishers who gave us permission to use that image on this site. The descriptions of these images will read something like: "reproduced with permission from...". If you want to use such items, you will have to ask the entity that holds the copyright. All material that is made by or for the Cardionetworks foundation is available for use and basis for your presentation according to a [http://creativecommons.org/licenses/by-nc/3.0/nl/deed.en_GB Creative Commons Attribution Noncommercial Share-Alike] license. If you cut the ECGpedia logo from a certain image, you will have to state elsewhere in the presentation that you obtained the material from ECGpedia, e.g. "'''ECG courtesy of Dr. Koster and ECGpedia.org'''". We do appreciate it when you [http://www.cardionetworks.org/contactCN.php let us know] that if you have used content from ECGpedia, just to have an idea who our audience is. <br />
<br />
;Can I use a certain image / animation / video / piece of text in a commercial presentation?<br />
:In general yes, but not without asking. In general we will not object you using any of our material as long as you do not copy-paste the whole website on a CD and sell it for money :-)... Please [http://www.cardionetworks.org/contactCN.php e-mail us for permission].<br />
<br />
;How can I use a flash movie from your site in my powerpoint presentation?<br />
:Read [http://www.adobe.com/go/tn_18822 this document] by Adobe to learn how.<br />
<br />
;When do I know enough to say that I can confidently interprete ECGs?<br />
:Of course, there is no definite answer to this question. However, the American College of Cardiology has published a list of [[ACC list|abnormalities a professional should be able to recognize]]. It is advisable to go through this list at the end of the course in order to recognize areas that need your attention. Understanding every item on the list does not guarantee that you will make the right decisions in every clinical situation.<br />
<br />
;Who are the people behind ECGpedia?<br />
:ECGpedia is an initiative of [http://cardionetworks.org Cardionetworks.org] a non-profit foundation whose goals is to advance medical knowledge, especially in the field of cardiology. The main contributors are: [[user:Drj|Jonas S.S.G. de Jong MD]], cardiology resident, author and moderator; [[user:Vdbilt|I.A.C. van der Bilt, MD]], cardiology resident, author and moderator; [[user:Tymen|Tymen T. Keller MD, PhD]], cardiology resident, author and moderator; [[user:Pgpostema|Pieter G. Postema MD]], cardiology research fellow, author and moderator; [http://www.medischeillustraties.nl Rob Kreuger], medical illustrator, made most of the drawings; and [[user:Bart|Bart Duineveld]], medical student, helps with technical issues, animations and lay-out.<br />
<br />
;My own ECG shows an abnormality what should I do?<br />
:The information on this site should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. For questions like these we advise you to contact your physician.<br />
<br />
;Can I trust the information on your site?<br />
{{ECGpedia:General_disclaimer}}<br />
<br />
;Do you protect the privacy of the patients whose ECGs / images / cases are presented?<br />
{{ECGpedia:Privacy_policy}}<br />
<br />
;What is the financial source of this project?<br />
:The [http://cardionetworks.org Cardionetworks.org] foundation is a non-profit charity foundation. The content of all websites maintained by the cardionetworks foundation is not influenced by sponsors. As the foundation was only recently started, no outside sources of funding have been contacted and the foundation has been funded privately by the founders. Feel free to [http://www.cardionetworks.org/contactCN.php contact the foundation] if you would like to sponsor or have sponsorship suggestions. We do not allow any advertisements on our sites. We also do not allow sponsors to influence any contents.<br />
<br />
;How can I contact you?<br />
:Please contact the [http://www.cardionetworks.org/contactCN.php secretary of Cardionetworks] for any further questions.<br />
<br />
;How can I contribute content to ECGpedia?<br />
{{:Contribute to ECGpedia}}<br />
<br />
We subscribe to the [http://www.hon.ch/HONcode/Conduct.html?HONConduct571624 HONcode] principles of the Health On the Net Foundation. [[Image:HONConduct571624.jpg]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Basics&diff=5624
Basics
2007-12-26T05:18:21Z
<p>195.229.242.57: relact</p>
<hr />
<div>litroctar<br />
noormonn<br />
{{nav|<br />
|previouspage=Introduction<br />
|previousname=Introduction<br />
|nextpage=Rate<br />
|nextname=Step 1: Heart Rate<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|editor= <br />
}}<br />
==How do I begin to read an ECG?==<br />
[[Image:nsr.png|thumb| A short ECG registration of normal heart rhythm (sinus rhythm)]]<br />
[[Image:Normaal ecg.jpg|thumb| An example of a normal ECG. ''Click on the Image for an enlargement'']]<br />
<br />
Click on the ECG to see an enlargement.<br />
Where do you start when interpreting an ECG?<br />
* on the top left are the patient's information, name, sex and date of birth<br />
* at the right of that are below each other the [[Frequency]], the [[Conduction|conduction times]] (PQ,QRS,QT/QTc), and the [[heart axis]] (P-top axis, QRS axis and T-top axis)<br />
* further to the right is the interpretation of the ECG written (this often misses in a 'fresh' ECG, but later the interpretation of the cardiologist or computer will be added)<br />
* down left is the 'paper speed' (25 mm/s on the horizontal axis), the sensitivity (10mm/mV) and the filter's frequency (40Hz, filters noise from eg. lights)<br />
* finally there is a calibration on the ECG, on the beginning of every lead is a vertical block that shows with what amplitude a 1 mV signal is drawn. So the height and depth of these signals are a measurement for the voltage. If this is not the set at 10 mm, there is something wrong with the machine setting.<br />
* further we have the ECG leads themselves of course, these will be discussed below.<br />
<br />
Note that the lay-out is different for every machine, but most machines will show the information above somewhere.<br />
{{clr}}<br />
<br />
==What does the ECG register?==<br />
An ECG is a registration of the heart's electric activity.<br />
Just like skeletal muscles, the heart is electrically stimulated to contract. This stimulation is also called ''activation'' or ''excitation''. Cardiac muscles are electrically charged at rest. The inside of the cell is negatively charged relative to the outside (resting potential). If the cardiac muscle cells are electrically stimulated they depolarize (the resting potential changes from negative to positive) and contract.<br />
As the impulse spreads through the heart, the electric field changes continually in size and direction. The ECG is a graphical visualisation of these electric signals in the heart.<br />
<br />
==The ECG represents the sum of the action potentials of millions of cardiomyocytes==<br />
{| class="wikitable" align="right" width=385px font-size="70%"<br />
|- <br />
!<flash>file=Single_cardiomyocyte.swf|width=382|height=315|quality=best|align=right||</flash><br />
|-<br />
| This movie shows the contraction of a single (rabbit) heart cell. The glass electrode measures the electrical current in the heart cell (with the[[w:Patch_clamp|patch-clamp method]]). The electrical signal is written in blue and shows the actionpotential. ''Courtesy of Arie Verkerk and Antoni van Ginneken, AMC, Amsterdam, The Netherlands''.<br />
|-<br />
|}<br />
[[Image:Hart_cells_en.png|thumb|The heart consists of approximately 300 trillion cells]]<br />
[[Image:cells_in_rest_en.png|thumb|In rest the heart cells are negatively charged. Through the depolarization by surrounding cells they become positively charged and they contract.]]<br />
[[Image:Ion_currents_en.png|thumb|During the depolarization sodium-ions stream inwards the cell. Subsequently the calcium-ions stream into the cell. These calcium-ions give the actual muscular contraction. Finally the potassium-ions stream out of the cell. During the repolarisation the ion concentration is corrected. On the ECG, an action potential wave coming towards the electrode is shown as a positive (upwards) signal. Here the ECG electrode is represented as an eye.]]<br />
The individual [[action potential|action potentials]] of the individual cardiomyocytes are averaged. The final result which is shown on the ECG is actually the average of trillions of microscopic electronical signals.<br />
{{clr}}<br />
<br />
==The electric discharge of the heart==<br />
[[Image:conduction_system_en.png|thumb]]<br />
<flash>file=Normal_SR.swf|width=300|height=400|quality=best|align=right||</flash><br />
'''The sinal node (SA node) contains pacemakercells which determine the heart frequency.'''<br />
'''First the [[heart|atria]] depolarise and contract, after that the [[heart|ventricles]]'''<br />
The electrical signal between the atria and the ventricles goes from the sinus node, via the atria to the AV-node (atrioventricular transition) to the His bundle and subsequently to the right and left bundle branch, which end in a dense network of Purkinje fibers.<br />
{{clr}}<br />
<br />
==The different ECG waves==<br />
[[Image:PQRS_origin_en.png|thumb| The origin of the different waves on the ECG]]<br />
[[Image:Epi_endo_en.png|thumb| The QRS complex is formed by the sum of the electric avtivity of the inner (endocardial) and the outer (epicardial) cardiomyocytes]]<br />
[[Image:Qrs-shapes.png|thumb| Example of the different QRS configuations]] <br />
The [[P_wave_morphology|'''P wave''']] is the result of the atrial depolarization. This depolarization starts in the SA (sino-atrial) node. The signal produces by pacemakercells in the SA node is conducted by the conduction system to the right and left atria. Normal atrial repolarisation is not visible on the ECG (but can be visible during [[atrial infarction]] and [[pericarditis]]). <br />
<br />
The [[QRS_morphology|'''QRS complex''' ]] is the average of the depolarization waves of the inner (endocardial) and outer (epicardial) cardiomyocytes. As the endocardial cardiomyocytes depolarize slightly earlier than the outer layers, a typical QRS pattern occurs (figure). <br />
<br />
The [[ST_morphology|'''T wave''']] represents the repolarisation of the ventricles. There is no cardiac muscle activity during the T wave.<br />
<br />
One heart beat consists of an atrial depolarization --> atrial contraction --> p-wave, ventricular depolarization --> ventricular contraction --> ORS-complex and the resting phase (including the repolarization during the T-wave) between two heart beats.<br />
<br />
Have a look at this excellent [[http://www-medlib.med.utah.edu/kw/pharm/hyper_heart1.html animation of the heart cycle]]<br />
<br />
The origin of the '''U wave''' is unknown. This wave possibly results from "afterdepolarizations" of the ventricles.<br />
<br />
The letters "Q", "R" and "S" are used to describe the QRS complex:<br />
*Q: the first negative deflection after the p-wave. If the first deflection is not negative, the Q is absent.<br />
*R: the positive deflection<br />
*S: the negative deflection after the R-wave<br />
<br />
*small print letters (q, r, s) are used to describe deflections of small amplitude. For example: qRS = small q, tall R, deep S. <br />
*R`: is used to describe a second R-wave (as in a [[right bundlebranch block]])<br />
See figure for some examples of this.<br />
{{clr}}<br />
<br />
==The history of the ECG==<br />
[[Image:Einthoven.gif|thumb|[[w:Einthoven|Willem Einthoven (1860-1927), the founder of the current ECG]]]]<br />
[[Image:einthECG1.png|thumb|ECG from Eindhoven's first publication. ''Pfügers Archiv March 1895, page 101-123'']]<br />
[[Image:stringgalvanometer.jpg|thumb|Einthoven's string-galvanometer, now in the Science Museum in Londen. The patient had to put his hands in salt baths to which the electrodes were connected. ''Image from the [http://www.ieee.org/portal/cms_docs_iportals/iportals/aboutus/history_center/conferences/che2004/Landman.pdf IEEE history society]''.]]<br />
[[Image:modern_ecg.jpg|thumb|The last generation of ECG equipment. Image courtesy of [http://www.gehealthcare.com/euen/cardiology/ General Electric]]]<br />
The history of the ECG goes back more than one and a half century<br />
<br />
In '''1843''' Emil Du Bois-Reymond, a german physiologist, was the first to describe "action potentials" of muscular contraction. He used a highly sensitive galvanometer, which contained more than 5 km of wire. Du Bios Reymond named the different waves: "o" was the stable equilibrium and he was the first to use the p, q, r and s to describe the different waves. <cite>Dubois</cite> However, in his excellent paper on the 'Naming of the waves in the ECG' Dr Hurst credits Einthoven for being the first to use PQRS and T.<cite>Hurst</cite><br />
<br />
In '''1850''' M. Hoffa described how he could induce irregular contractions of the ventricles of doghearts by administering electrical shock. <cite>Hoffa</cite><br />
<br />
In '''1887''' the English physiologist Augustus D. Waller from Londen published the first human electrocardiogram. He used a capillar-electrometer. <cite>Waller</cite><br />
<br />
[[w:Einthoven|The dutchman Willem Einthoven]] (1860-1927) introduced in 1893 the term 'electrocardiogram'. He described in '''1895''' how he used a galvanometer to visualize the electrical activity of the heart. In 1924 he received the Nobelprize for his work on the ECG. He connected electrodes to a patienta showed the electrical difference between two electrodes on the galvanometer. We still now use the term: Einthovens'leads. The string galvanometer (see Image) was the first clinical instrument on the recording of an ECG.<br />
<br />
In 1905 Einthoven recorded the first 'telecardiogram' from the hospital to his laboratoy 1.5 km away.<br />
<br />
In 1906 Einthoven published the first article in which he described a series of abnormal ECGs: left- and right bundlebranchblock, left- and right atrialdilatation, the U wave, notching of the QRS complex, ventricular extrasystoles, bigemini, atrialflutter and total AV block. <cite>Einthoven</cite><br />
{{clr}}<br />
<br />
==The ECG electrodes==<br />
[[Image:ECGelectrodes.jpg|thumb|click on the Image for an enlargement]]<br />
Electric activity going through the heart, can be measured by external (skin)electrodes. The electrocardiogram (ECG) registers these activities from these electrodes which have been attached on diffrent places on the body. In total, twelve leads are calculated using ten electrodes.<br />
<br />
The ten electrodes are:<br />
* '''the extremity electrodes:'''<br />
** LA - left arm<br />
** RA - right arm<br />
** N - neutral, on the right leg (= electrisch aarde of nulpunt ten opzichte waarvan de electrische spanning wordt gemeten)<br />
** F - foot, on the left leg<br />
It makes no difference whether the electrodes are attached proximal or distal on the extremities. ''However'', it is best to be uniform in this. (eg. do not attach an electrode on the left shoulder and one on the right wrist).<br />
<br />
* '''the chest electrodes:'''<br />
** V1 - placed in the 4th intercostal space, right of the sternum<br />
** V2 - placed in the 4th intercostal space, left of the sternum<br />
** V3 - placed between V2 and V4<br />
** V4 - placed 5th intercostal space in the nippleline. Official recommendations are to place V4 under the breast in women.<cite>Kligfield</cite><br />
** V5 - placed between V4 and V6 <br />
** V6 - placed in the midaxillary line on the same height as V4 (horizontal line from V4, so not necessarily in the 5th intercostal space)<br />
<br />
{{clr}}<br />
<br />
Using these 10 electrodes, 12 leads can be derived. There are 6 extremity leads and 6 precordial leads.<br />
===The Extremity Leads===<br />
[[Image:ECGafleidingen.jpg|thumb]]<br />
The extremity leads are:<br />
<br />
*'''I''' from the right to the left arm<br />
*'''II''' from the right arm to the left leg<br />
*'''III''' from the left arm to the left leg<br />
An easy rule to remember: lead '''I''' + lead '''III''' = lead '''II'''<br />
This is done with the use of the height or depth, independent of the wave (QRS, P of T).<br />
Example: if in lead I, the QrS complex is 3 mm in height and in lead III 9mm, the height of the QRS-complex in lead II is 12mm.<br />
<br />
Other extremity leads are:<br />
<br />
*'''AVL''' points to the left arm<br />
*'''AVR''' points to the right arm <br />
*'''AVF''' points to the feet<br />
<br />
The capital A stands for "augmented" and V for "voltage".<br />
<br />
(aVR + aVL + aVF = 0)<br />
{{clr}}<br />
<br />
===The Chest Leads===<br />
The precordial, or chestleads, '''(V1,V2,V3,V4,V5 and V6)''' 'observe' the depolarization wave in the frontal plane<br />
<br />
''Example'': V1 is close to the right ventricle and the right atrium. Signals in these areas of the heart have the largest signal in this lead. V6 is the closest to the lateral wall of the left ventricle.<br />
<br />
===Special Leads===<br />
In case of an inferior wall infarct, extra leads may be used:<br />
#In a right side ECG, V1 and V2 remain on the same place.V3 to V6 are placed on the same place but mirrored on the chest. So V4 is in the middle of the right clavicle. On the ECG it should be marked that it is a ''Right sided ECG''. V4R (V4 but right sided) is a sensitive lead to diagnose right ventricular infarction.<br />
#Leads V7-V8-V9 can be used to diagnose a posteriorinfarct. It is means that after V6, leads are pkaced towards the back. See the chapter[[Ischemia]] for other ways of diagnosing posterior infarction.<br />
<br />
{{:Technical Problems}}<br />
<br />
==References==<br />
<biblio><br />
#Dubois Du Bois-Reymond, E. ''Untersuchungen über thierische Elektricität''. Reimer, Berlin: 1848.<br />
#Hoffa Hoffa M, Ludwig C. 1850. ''Einige neue versuche uber herzbewegung''. Zeitschrift Rationelle Medizin, 9: 107-144<br />
#Waller Waller AD. ''A demonstration on man of electromotive changes accompanying the heart's beat.'' J Physiol (London) 1887;8:229-234<br />
#Einthoven Einthoven W. ''Le telecardiogramme''. Arch Int de Physiol 1906;4:132-164<br />
#Einthoven2 Einthoven W. ''ÃÂber die Form des menschlichen Electrocardiogramms''. Pfügers Archiv maart 1895, pagina 101-123<br />
#Marey Marey EJ. ''Des variations electriques des muscles et du couer en particulier etudies au moyen de l'electrometre de M Lippman.'' Compres Rendus Hebdomadaires des Seances de l'Acadamie des sciences 1876;82:975-977 <br />
#Marquez pmid=12177632<br />
#Hurst pmid=9799216<br />
#Kligfield pmid=17322457<br />
</biblio><br />
<br />
==External links==<br />
*[http://www.ecglibrary.com/ecghist.html An extensive history of the ECG]<br />
<br />
[[nl:Grondbeginselen]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Chamber_Hypertrophy_and_Enlargment&diff=5623
Chamber Hypertrophy and Enlargment
2007-12-26T05:17:30Z
<p>195.229.242.57: lidelcov</p>
<hr />
<div>taacvarlisi<br />
oueltdar<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
In hypertrophy the heart muscle is thicker. This can have different causes. Left ventricular hypertrophy results from an increase in left ventricular workload, e.g. during hypertension or aortic valve stenosis. Right ventricular hypertrophy results from an increase in right ventricular workoad, e.g. emphysema or pulmonary embolisation. <br />
These causes are fundamentally different from [[Miscellaneous#Hypertrophic_Obstructive_Cardiomyopathy|hypertrophic obstructive cardiomyopathy (HCM)]], which is a congenital misallignment of cardiomyocytes resulting in hypertrophy. <br />
<br />
Left and right ventricular hypertrophy can be distinguished on the ECG:<br />
<br />
==Left ventricular hypertrophy==<br />
[[Image:E_lvh.jpg|thumb|LVH. R in V5 is 26mm, S in V1 in 15mm. The sum is 41 mm which is more than 35 mm and therefore LVH is present according to the Sokolow-Lyon criteria.]]<br />
[[Image:linker_ventrikel_hypertrofie.GIF|thumb]]<br />
<br />
As the left ventricular becomes thicker, the QRS complexes become larger. This is especially true for leads V1-V6. The S wave in V1 is deep, the R wave in V4 is high. Often some ST depression can be seen in leads V5-V6, which is in this setting is called a 'strain pattern'.<br />
<br />
To diagnose left ventricular hypertrhophy on the ECG one of the following criteria should be met:<br />
*R in V5 or V6 + S in V1 >35 mm. (this is called the '''Sokolow-Lyon criterium'''<cite>Sokolow</cite>)<br />
*R >26 mm in V5 or V6; <br />
*R >20 mm in I, II or III; <br />
*R >12 mm in aVL (in the absence of [[Conduction delay#LAFB|left anterior fascicular block]]);<br />
<br />
The '''Cornell-criterium''' has different values in men and women:<br />
* R in aVL and S in V3 >28 mm in men<br />
* R in aVL and S in V3 >20 mm in women<br />
<br />
Left ventricular hypertrophy has prognostic consequences as has been found in several studies.<cite>Levy</cite><cite>Sundstrom</cite><br />
<br />
===Examples===<br />
<gallery><br />
Image:LVH.jpg|ECG of patient with left ventricular hypertrophy according to the Sokolow-Lyon criteria<br />
Image:Extreme_lvh2.jpg|Another example of extreme left ventricular hypertrophy in a patient with severe aortic valve stenosis.<br />
Image:extreme_lvh.jpg|ECG of a patient with LVH and subendocardial ischemia leading to positive cardiovascular markers in blood testing.<br />
</gallery><br />
{{clr}}<br />
<br />
==Right ventricular hypertrophy==<br />
[[Image:Rechter_ventrikel_hypertrofie.GIF|thumb]]<br />
[[Image:E_rvh.jpg|thumb|Right ventricular hypertrohpy, the R wave is greater than the S wave in V1]]<br />
Right ventricular hypertrophy occurs mainly in lung disease or in congenital heart disease. <br />
The ECG shows a negative QRS complex in I (and thus a right [[heart axis]]) and a positive QRS complex in V1.<br />
<br />
*R > S in V1 (R must be > 0.5 mV) <br />
*Right [[heart axis]]<br />
{{clr}}<br />
<br />
==Left atrial enlargement==<br />
;Criteria for left atrial voor left atrial enlargement. Either<br />
:P wave with a broad (>0,04 sec or 1 small square) and deeply negative (>1 mm) terminal part in V1<br />
:P wave duration >0,12 sec in laeds I and / or II<br />
[[Image:left_atrial_enlargement.jpg|thumb| Left atrial enlargement]]<br />
[[Image:LAE_2.png|thumb| Left atrial enlargement with ECG.]]<br />
[[Image:ECG_LAtrD_v1.jpg|thumb| Left atrial enlargement as seen in lead V1.]]<br />
Left atrial enlargement is often seen in mitral valve insufficiency, resulting in backflow of blood from the left ventricle to the left atrium and subsequent incresed local pressure. <br />
{{clr}}<br />
<br />
==Right atrial enlargement==<br />
;Right atrial enlargement is defined as either:<br />
:P >2,5 mm in II / III and / or aVF <br />
:P >1,5 mm in V1.<br />
[[Image:right_atrial_enlargement.jpg|thumb| Right atrial enlargement]]<br />
[[Image:Rae.png|thumb| Right atrial enlargement]]<br />
Right atrial enlargement can result from increased pressure in the pulmonary artery, e.g. after pulmonary embolisation. A positive part of the biphasic p-wave in lead V1 larger than the negative part indicates right atrial enlargement. The width of the p wave does not change. <br />
{{clr}}<br />
<br />
==Biatrial enlargement==<br />
;Biatrial enlargement<br />
:Biphasic p wave in V1 of more than 0.04 sec duration. The positive initial part is > 1.5mm and the negative terminal part > 1mm<br />
In biatrial enlargement is the ECG whos signs of both left and right atrial enlargement. In V1 the p wave has large peaks first in positive and later in negative direction.<br />
<br />
==References==<br />
<biblio><br />
#Sokolow Sokolow M, Lyon TP: ''The ventricular complex in left verntricular hypterfophy as obtained by unipolar precordial and limb leads.'' Am Heart J 37: 161, 1949<br />
#Levy pmid=11352882<br />
#Sundstrom pmid=7923663<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Pacemaker&diff=5622
Pacemaker
2007-12-26T05:17:04Z
<p>195.229.242.57: acellacz</p>
<hr />
<div>bopasre<br />
erreltarelm<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
[[Image:picture_pacemaker.jpg|thumb|A (used) DDDr pacemaker]]<br />
[[Image:paced2.gif|thumb| Ventricular paced rhythm shows ventricular pacemaker spikes]]<br />
[[Image:Pacemaker2.jpg |thumb| VVI pacemaker rhythm. Note the LBBB morphology with left axis deviation indicating the pacing lead in the right ventricular apex.]]<br />
<br />
<br />
A pacemaker is indicated when the electrical impulse conduction or formation is dangerously disturbed. The paced '''pacemaker rhythm''' can easily be recognized on the ECG as it shows '''pacemaker spikes''': vertical signals that represent the electrical activity of the pacemaker.<br />
<br />
In the first example image, the atria are being paced, but not the ventricles, resulting in a '''atrial paced rhythm'''. Accordingly the ventricular beat is delayed until the atrial signal has passed the AV node. In the second image the ventricles are paced directly, resulting in '''ventricular paced rhythm'''. As ventricular pacing occurs exclusively in the right ventricle the ECG shows a left bundle branch pattern. An exception to this rule is left ventricular pacing in patients with congenital anomalies and patients with an epicardial pacemaker that has been placed during surgery.<br />
<br />
===Pacemaker Coding===<br />
Pacemakers can be categorized according to the NASPE coding system, that usually consists of 3-5 letters. <br />
* The first letter represents the chamber where the signal is "sensed": O=none, A=atria, V=ventricle, D=dual (atrial and / or ventricle)<br />
* The second letter represents the chamber that is being paced: A=atria, V=ventricle, D=dual (atria and / or ventricle)<br />
* The third letter represents the action that follows the sensed signal: O = none, T = triggered, I = inhibited (i.e. if the heart beats by itself, the pacemaker is silent) and D = dual (T + I). <br />
* The fourth letter denotes whether the pacemaker has a fixed rate (0 = none) or has rate modulation (R).<br />
* The fifth letter indicates whether the pacemaker can pace both the atria and right chamber. This letter is seldomly used.<br />
<br />
===Commonly Used Pacemakers===<br />
The most often used codes are:<br />
* '''AAI''': the atria are paced, when the intrinsic atrial rhythm falls below the pacemakers threshold<br />
* '''VVI''': the ventricles are paced, when the intrinsic ventricular rhythm falls below the pacemakers threshold<br />
* '''DDD''': the pacemaker records both the atrial and ventricular rate and can pace one of each chambers when needed.<br />
* '''DDDR''': as above, but the pacemaker has a sensor that records a demand for higher cardiac output and can adjust the heart rate accordingly.<br />
* Biventricular pacemakers ('''CRT-D'''): leads in both ventricles are present to synchronize contraction. This cardiac synchronization therapy can improve symptoms and survival in some heart failure patients. <br />
* '''[[ICD]]''' (Internal Cardioversion Device): this device can detect and treat [[Ventricular Tachycardia]] and [[Ventricular Fibrillation]]. Usually the first treatment is anti-tachy pacing (pacing at a rate +- 10% above the ventricular rate in ventricular tachycardia, which can convert the rhythm to sinus rhythm). If this is not effective an defibrillator shock is delivered, usually with 16-36 Joules of energy. ICDs can save lives in patients who have a high risk of ventricular arrhythmias. All ICDs have optional pacemaker activity to treat bradycardias. New biventricular ICDs have 3 leads: an atrial lead, a left ventricular lead and a right ventricular lead.<br />
<br />
===Pacemaker Indications===<br />
A full list of pacemaker indications can be read in the ESC guidelines on cardiac pacing <cite>Vardas</cite>. A selection of class I indications are: chronic symptomatic third- or second degree (Mobtiz I or II) atrioventricular block. Syncope with sinus node disease. Alternating bundle branch block. Persisting AV block after surgery.<br />
<br />
===ICD Indications===<br />
<br />
===Atrial-sensed ventricular-paced rhythm===<br />
===AV dual-paced rhythm===<br />
===Pacemaker Malfunction===<br />
to be filled in ...<br />
====Failure of appropriate capture, atrial====<br />
====Failure of appropriate capture, ventricular====<br />
====Failure of appropriate inhibition, atrial====<br />
====Failure of appropriate inhibition, ventricular====<br />
====Failure of appropriate pacemaker firing====<br />
====Retrograde atrial activation====<br />
====Pacemaker mediated tachycardia====<br />
<br />
==External Links==<br />
[http://www.hrsonline.org/swPositionStatementFiles/ps101036428.asp Heart Rhytm Society]<br />
<br />
<br />
==References==<br />
<biblio><br />
#Vardas pmid=17726042<br />
#Gregoratos pmid=12379588<br />
</biblio><br />
<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Supraventricular_Rhythms&diff=5621
Supraventricular Rhythms
2007-12-26T05:16:36Z
<p>195.229.242.57: ologetc4t</p>
<hr />
<div>siteracgetol<br />
acereltaceld<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
'''Supraventricular Rhythms originate from the atria. Examples of supraventricular rhythms are:'''<br />
*[[Sinustachycardia]]<br />
*[[Atrial Rhythm]]<br />
*[[Atrial Flutter]]<br />
*[[Atrial Fibrillation]]<br />
*[[Atrial Tachycardia]]<br />
*[[AVRT|Atrio-ventricular Reentry Tachycardia AVRT]]<br />
<br />
'''Supraventricular [[Ectopic Beats|ectopic beats]] can result in:'''<br />
*[[Atrial Premature Complexes]]<br />
*[[Wandering Pacemaker]]<br />
*[[AV-nodal complexes]]<br />
<br />
'''Also read:'''<br />
*Flowchart: [[Media:narrow_tachycardia_flow.png|Approach to the Narrow Complex Tachycardia]] Adapted from <cite>ESCnarrowQRS</cite>.<br />
*[[Introduction to Arrhythmias]]<br />
*[[Mechanisms of Arrhythmias]]<br />
*[[Sinus node rhythms and arrhythmias]]<br />
*[[Junctional Tachycardias]]<br />
*[[Ventricular Arrhythmias]]<br />
<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''An overview of supraventricular tachycardias'''<br />
|-<br />
!<br />
!regularity<br />
!atrial frequency<br />
!ventricular frequency<br />
!origin (SVT/VT)<br />
!p-wave<br />
!effect of adenosine<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Narrow complex (QRS<0.12)'''<br />
|-<br />
! [[Sinustachycardia]]<br />
| regular<br />
| 100-180 bpm<br />
| 100-180 bpm<br />
| sinusnode (SVT)<br />
| precedes every QRS complex<br />
| gradual slowing<br />
|-<br />
! [[Atrial Fibrillation]]<br />
| grossly irregular<br />
| 400-600 bpm <br />
| 75-175 bpm <br />
| atria (SVT)<br />
| absent<br />
| slows down rate; irregularity remains<br />
|-<br />
! [[Atrial Flutter]]<br />
| regular (sometimes alternating block) <br />
| 250-350 bpm <br />
| 75-150 bpm (3:1 or 2:1 block is most common) <br />
| atria (SVT)<br />
| negative sawtooth in lead II <br />
| temporary reduced conduction (e.g. 4:1)<br />
|-<br />
! [[AVNRT]] <br />
| regular <br />
| 180-250 bpm<br />
| 180-250 bpm <br />
| AV-node (SVT)<br />
| in QRS complex (R') <br />
| stops<br />
|-<br />
! [[Atrial Tachycardia]]<br />
| regular<br />
| 120-250 bpm <br />
| 75-200 bpm<br />
| atria<br />
| precedes QRS, p wave differs from sinus-p <br />
| temporary AV-block<br />
|-<br />
! [[AVRT|Atrio-Ventricular Reentry Tachycardia (AVRT)- orthodromic]]<br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circle: av-node - ventricles - bypass - atria<br />
| RP < PR <br />
| stops<br />
|-<br />
! [[AVJT|AV junctional tachycardia]]<br />
| regular <br />
| 60-100 bpm<br />
| 70-130 bpm<br />
| AV node<br />
| RP < PR <br />
| reduces rate<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Wide complex (QRS>0.12)'''<br />
|-<br />
! [[Supraventricular tachycardia with block]]<br />
| (ir)regular depending on SVT<br />
| 150-250 bpm<br />
| 75-200 bpm<br />
| atria (SVT)<br />
| absent<br />
| temporary increased AV-block (eg 4:1)<br />
|-<br />
! [[AVRT|Atrio-ventricular Reentry Tachycardia (AVRT) - antidrome]]<br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circular: bypass - atria - av-node - ventricles<br />
| RP < PR <br />
| stops<br />
|-<br />
|}<br />
<br />
==References==<br />
<biblio><br />
#ESCnarrowQRS pmid=14563598<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Introduction&diff=5620
Introduction
2007-12-26T05:15:56Z
<p>195.229.242.57: erlalirac</p>
<hr />
<div>bocaleltric<br />
noaceleltl<br />
{{nav|<br />
|previouspage=/<br />
|previousname=/<br />
|nextpage=Basics<br />
|nextname=Basics<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= <br />
}}<br />
[[Image:nsr.png|thumb| A short ECG registration of normal heart rhythm (sinus rhythm)]]<br />
The aim of this course is to understand and recognize the normal ECG and to be able to interprete abnormalities. The course is divided in two different sections. First the [[basics]] will be presented. This is followed by the interpretation of the normal ECG according to the 7+2 step plan:<br />
* Step 1: [[Rhythm]]<br />
* Step 2: [[Rate]]<br />
* Step 3: [[Conduction]] (PQ,QRS,QT)<br />
* Step 4: [[Heart axis]]<br />
* Step 5: [[P wave morphology]]<br />
* Step 6: [[QRS morphology]]<br />
* Step 7: [[ST morphology]]<br />
* Step 7+1: [[Compare_the_old_and_new_ECG|Compare the current ECG with a previous one]]<br />
* Step 7+2: [[Conclusion]]<br />
<br />
<br />
Finally the real world is presented through [[Cases and Examples|practice ECGs]].<br />
<br />
If you have finished the course you are invited to come back to read more about abnormal ECGs in the ECG textbook.<br />
<br />
Also read our [[Frequently Asked Questions]] section.<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Rate&diff=5619
Rate
2007-12-26T05:15:31Z
<p>195.229.242.57: taoloacca</p>
<hr />
<div>altaerdelb<br />
alrolcole<br />
{{nav|<br />
|previouspage=Rhythm<br />
|previousname=Step 1: Rhythm<br />
|nextpage=Conduction<br />
|nextname=Step 3:Conduction intervals (PQ, QRS, QT, QTc)<br />
}}<br />
==What is the heart rate?==<br />
[[Image:ECGpapier.png|thumb| The width of a square on the ECG represents time]]<br />
[[Image:Ecgfreq.png|thumb| The countmethod to determine the heartfrequency. The second QRS-complex is between ''75'' and ''60'' beat per minute. This heartbeat is between that, around 65 beats per minute.]]<br />
<br />
To anwer this question, determine the time between two QRS complexes. Previously, the ECG was registered on a paperstrip transported through an ECG writer at the speed of 25 mm/second. Nowadays, digital ECG registration is common however, the method of determining the frequency remains the same. The ECG paper has a grid with thick lines 5 mm apart (= 0,20 second) and thin lines 1 mm (0,04 second). <br />
<br />
<br />
'''There are three simple methods to determine the heart rate (HR):'''<br />
# Count the small (1mm) squares between two QRS-complexes. Hense, the ECG paper runs with 25 mm/sec through the ECG writer, therefore:&nbsp;&nbsp;&nbsp;[[Image:HFformule_en.png]]This method works well in case of tachycardia (>100 beats/minute)<br><br />
# To determine the frequency of a normal sinus ritme: Use the sequence 300-150-100-75-60-50-43-37. Count from the first QRS complex, the first thick line is 300, the next line 150 etc. Stop the sequence at the next QRS complex. When the second QRS complex is in between two lines, take the mean of the two numbers from the sequence or use the finetune method listed to the right.<br />
# Non regular rhytms are best determined with the "3 second marker method" Count the number of QRS-complexes that fit in 3 seconds (some ECG writers register this period on the ECG paper). Multiply this number by 20 and find the number of beats/minute. <br />
{{clr}}<br />
{| class="wikitable" font-size="90%" align="right" <br />
|+'''The 'square counting' method can be finetuned with the following sequence'''<br />
|-<br />
|'''300'''||250||214||187||167||'''150'''||136||125||115||107||'''100'''||94||88||83||79||'''75'''||71||68||65||62||'''60'''<br />
|-<br />
|}<br />
{{clr}}<br />
<br />
==What changes the frequency of the heart?==<br />
A number of factors change the heart frequency including:<br />
* the (para) sympathic nerve system. <br />
** The '''sympathic system''' e.g. epinephrin (=adrenalin) increases the atrioventricular conduction and contractility. (the ''fight, fright, flight'' reaction)<br />
** The parasympathic system (nervus vagus) e.g. acetycholin decreases the frequency and atrioventricular conduction. The parasympathic system effects mainly the atria.<br />
* Cardiac filling increases the frequency.</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=QRS_axis&diff=5618
QRS axis
2007-12-26T05:15:14Z
<p>195.229.242.57: monorvarsito</p>
<hr />
<div>trdroncao<br />
boctroccn<br />
{{nav|<br />
|previouspage=Conduction<br />
|previousname=Step 3: Conduction (PQ, QRS, QT, QTc)<br />
|nextpage=P_wave_morphology<br />
|nextname=Step 5: P wave morphology<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor= <br />
}}<br />
<br />
==What is the electrical heartaxis?==<br />
[[Image:hartas2.jpg|thumb|The heartaxis indicates the average direction of the depolarization wave. A normal heartaxis, the picture shows an example, is between -30 and +90 degrees. In this example, the heartaxis is +45 degrees.]]<br />
[[Image:einthhartas.png|thumb|Heartaxis from the original publication of Einthoven. Reprinted from The Lancet, March 30 1912, Einthoven W.,<br />
''The Different Forms of The Human Electrocardiogram and Their Signification'', 853-861, 1912, with permission from<br />
Elsevier]]<br />
The electrical heartaxis is an average of all depolarizations in the heart. The depolarization wave begins in the right atrium and proceeds to the left and right ventricle. Because the left ventricle wall is thicker than the right wall, the arrow indicating the direction of the depolarization wave is directed to the left.<br />
<br />
For a lot of people, this is a difficult concept. The theoretic part seems difficult but by doing it a lot, it will become clear.<br />
{{clr}}<br />
<br />
==How do you determine the electrical heartaxis==<br />
[[Image:hart_axis.png|thumb]]<br />
[[Image:hartasroset.png|thumb]]<br />
<br />
When you average all electrical signals from the heart, you can indicate the direction of the average electrical depolarization with an arrow (vector). This is the heartaxis. Especially a change of the heartaxis or an extreme deviation can be an indication for pathology.<br />
<br />
<i>For example:</i><br />
<br />
*Biggest QRS deflection in lead I: the electrical activity is directed to the left (of the patient)<br />
*Biggest QRS deflection in lead AVF: the electrical activity is directed down.<br />
<br />
This indicates a normal heartaxis. Usually, these two leads are enough to diagnose a normal heartaxis!<br />
<br />
The biggest vector in the heart is from the AV-node in the direction of the ventricular depolarization. Under normal circumstances, this is directed left and down.(towards leads I and AVF). The position of the QRS vector is given in degrees. See the figure, the middle of the figure is the AV-node. A horizontal line towards the left arm is defined as 0 degrees.<br />
<br />
A normal heartaxis is between -30 and +90 degrees.<br />
<br />
'''Rule:''' biggest QRS deflection in I and II is an intermediate = normal heartaxis. <br />
So positive deflections in I and II indicates a normal heartaxis.<br />
<br />
{{clr}}<br />
====Interpretation====<br />
The interpretation of the electrical heartaxis has a few rules of thumb:<br />
<br />
* First, when a positive depolarization wave moves towards a positive electrode, a positive, upwards deflection is registered on the ECG.<br />
*Second, there are 4 quadrants where the QRS-vector can point to:<br />
**left upper quadrant --> left axis deviation (between -30ú and -90ú)<br />
**left lower quadrant --> normal (between -30ú and 90ú)<br />
**right below and right --> right axis deviation (between 90ú and -150ú)<br />
**right upper quadrant --> extreme axis (between -90ú and -150ú)<br />
<br />
''Example'': <br />
<br />
The QRS in lead I, will have a negative deflection in a right axis deviation. The vector is not directed towards the electrode. However, lead AVF will be positive, the vector is directed towards the electrode.<br />
<br />
====Heart-axis Simulator====<br />
<br />
To understand how the ECG changes in axis deviations, this excellent axis-simulator may be helpful: http://www.blaufuss.org/ECGviewer/indexFrame2.html<br />
<br />
====Iso-electrical====<br />
'''Note:''' When the depolarization is perpendicular on the lead, this is called <br />
'''iso-electrical'''. The QRS is neither positive nor negative. <br />
<br />
====Undetermined axis ====<br />
When all extremity leads are biphasic, the axis is directed to the front or back, in a transverse plane. The axis is than '''undetermined'''.<br />
<br />
==Abnormal heartaxis==<br />
[[Image:left_axis_dev.jpg|thumb| Heartaxis deviation to the left in case of an inferior infarct. Left anterior hemi Block is a common cause. A left axis is between -30 and -90 degrees. The axis is -30 degrees.]]<br />
[[Image:right_axis_dev.jpg|thumb| Heartaxis deviation to the right in right ventricular load, as in COPD or pulmonary embolism. A right axis is between +90 and +180 degrees. In this case the axis is +135 degrees]]<br />
The direction of the vector can changes under different circumstances:<br />
<br />
#When the heart itself is rotated (right ventricular overload), obviously the axis turns with it. <br />
#In case of ventricular hypertrophy, the axis will deviate by the bigger electrical activity and the vector will turn towards the hypertrophied tissue. <br />
#Infarcted tissue is electrically dead. No electrical activity is registered and the QRS vector turns away from the infracted tissue<br />
#In conduction problems, the axis deviates too. When the right ventricle depolarizes later than the left ventricle, the axis will turn to the right (RBBB). This is because the right ventricle will begin the contraction later and therefore will also finish later. In a normal situation the vector is influenced by the left ventricle but now only by the right ventricle.<br />
<br />
{{clr}}<br />
<br />
==Examples of a left heartaxis==<br />
[[Image:LHA.png|thumb| Left heartaxis]]<br />
[[Image:LAHB.png|thumb| Left anterior hemi block]]<br />
*[[Conduction delay#LAFB| left anterior fascicular block]]<br />
*[[Ischemia#Inferior|Inferior myocardial infarction]]<br />
*[[Hypertrophy|Left ventricular hypertrophy]]<br />
*Pacemaker rhythm<br />
{{clr}}<br />
<br />
== Examples of a right heartaxis ==<br />
[[Image:rightaxis.jpg|thumb| Right heartaxis]]<br />
*[[Hypertrophy| Right ventricular hypertrophy]]<br />
*Right ventricular load, for example [[Pulmonary_Embolism|Pulmonary Embolism]] or Cor Pulmonale (as in COPD)<br />
*Atriumseptumdefect, ventricleseptumdefect<br />
{{clr}}<br />
<br />
==Microvoltages==<br />
{{:Microvoltages}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Technical_Problems&diff=5617
Technical Problems
2007-12-26T05:14:56Z
<p>195.229.242.57: ricpasli</p>
<hr />
<div>bascobo<br />
cnaouoloalou<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de Jong]]<br />
|supervisor= <br />
}}<br />
==Lead reversals==<br />
[[Image:cableReversal1.png|thumb|Right and left arm lead reversal can be distinguished from the (much rarer) dextrocardia by looking at the precordial R wave progression.]]<br />
[[Image:cableReversal2.png|thumb|Right arm and left leg lead reversal. Lead II now measures the signal between the left and right leg, which is remote from the heart.]]<br />
Sometimes an ECG is made properly. Mistakes do happen and leads can be switched. Always remain careful to check this or you might come to the wrong conclusions. One of the most common mistakes is to switch the right and left arm. This will result in negative complexes in I, indicating a right axis deviation!<br />
<br />
Common mistakes are reversal of:<br />
*right leg and right arm:<br />
**Hardly any signal in lead II.<br />
*right and left arm electrodes; <br />
**reversal of leads II and III<br />
**reversal of leads aVR and aVL<br />
*left arm and left leg:<br />
**reversal of leads I and II<br />
**reversal of leads aVR and aVF<br />
**inversion of lead III<br />
*right arm and left leg:<br />
**inversion of leads I, II and III<br />
**reversal of leads aVR and aVF<br />
<br />
<br />
It is possible to distinguish lead reversal and [[w:Dextrocardia|dextrocardia]] by watching the precordial leads. Dextrocardia will show an R wave inversion, wheras lead reversal will not.<br />
{{clr}}<br />
<br />
==Artefacts==<br />
[[Image:Noise_move.png|thumb| Movement artefacts]]<br />
[[Image:ECG_Parkinson.png|thumb| Increasing movement artefacts in a Parkinson patient. The patient was in sinus rhythm! (which doesn't show on this short recording)]]<br />
[[Image:BaselineDrift.png|thumb| Baseline drift. The amplifier in the ECG machine has to re-find the 'mean'. This often occurs right after lead connection and after electric cardioversion.]]<br />
[[Image:cardioversion_from_afib.jpg|thumb| Cardioversion from atrial fibrillation to sinusrhythm, with clear baseline drift.]]<br />
[[Image:electric_noise_ecg.png|thumb| Electrical interference from a nearby electrical appliance. A typical example is a 100 Hz background distortion from fluorescent lights. Not to be confused with [[arrhythmias#atrial fibrillation|atrial fibrillation]].]]<br />
[[Image:electric_noise_ecg2.jpg|thumb| Another example of an artefact caused by an electrical appliance. The patients rhythm is regular. This strip shows 10 QRS complexes.]]<br />
<br />
Artefacts (disturbances) can have many causes. Common causes are:<br />
*Movement <br />
*Electrical interference<br />
<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Electrolyte_Disorders&diff=5616
Electrolyte Disorders
2007-12-26T05:14:37Z
<p>195.229.242.57: dardomerlavi</p>
<hr />
<div>reltrocelco<br />
cnamondomcn<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor= <br />
}}<br />
===Hypercalcemia===<br />
Hypercalcemia results in a faster repolarization. Characteristics of hypercalcemia:<br />
*mild: broad based tall peaking T waves<br />
*severe: extremely wide QRS, low R wave, disappearance of p waves, tall peaking T waves.<br />
<br />
===Hypocalcemia===<br />
ECG-characteristics of hypocalcemia:<br />
*narrowing of the QRS complex<br />
*reduced PR interval<br />
*T wave flattening and inversion<br />
*prolongation of the QT-interval <br />
*prominent U-wave<br />
*prolonged ST and ST-depression<br />
<br />
===Hyperkalemia===<br />
[[Image:ecg_hyperkaliemie.jpg|thumb| Extreme hyperkalemia. No p-waves, wide QRS, tall peaking T waves.]]<br />
[[Image:ecg_hyperkaliemie2.jpg|thumb| Same patient after partial correction of the potassium level. Still no p-waves visible, wide QRS, tall peaking T waves.]]<br />
ECG characteristics of hyperkalemia:<br />
*Tall peaked T waves<br />
*Flattening p-waves. In extreme hyperkalemia p-waves may disappear altogether.<br />
*Prolonged depolarization leading to QRS widening (nonspecific intraventricular conduction defect) sometimes > 0.20 seconds<br />
<br />
At concentrations > 7.5 mmol/L atrial and [[Ventricular Fibrillation|ventricular fibrillation]] can occur.<br />
{{clr}}<br />
<br />
===Hypokalemia===<br />
[[Image:KJcasu18-3.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. ECG1]]<br />
[[Image:KJcasu18-2.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. ECG2]]<br />
[[Image:KJcasu18-1.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. After correction of potassium levels.]]<br />
Hypokalemia is a low blood potassium level. This results in:<br />
*ST depression and flattening of the T wave<br />
*Negative T waves<br />
*A U-wave may be visible<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Introduction_to_Arrhythmias&diff=5615
Introduction to Arrhythmias
2007-12-26T05:14:18Z
<p>195.229.242.57: reldomcnare</p>
<hr />
<div>zelalalvarc<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
[[Image:VT_SVT_LBBB_WCT.svg|thumb|Morphologic criteria to differentiate between SVT vs. VT in a wide complex tachycardia. This is part of the [[media:wideQRS_tachycardia_flow.png|wide complex tachycardia flowchart]]]]<br />
Arrhythmias (non-normal heart rhythms) can be a challenge to the person who tries to understand them. But with a systematical approach, diagnosis is often less difficult than it seems at the beginning.<br />
<br />
'''First look at the heart rate:'''<br />
*>100 bpm = tachycardia<br />
*<60 bpm = bradycardia<br />
*are there extra beats? -> [[Ectopic Beats]]<br />
<br />
Secondly it is important to assess the '''origin of the arrhythmia''':<br />
*If the QRS < 120ms (i.e. a narrow complex), then it is either a [[Sinus node rhythms and arrhythmias|sinus arrhythmia]], [[Supraventricular Rhythms|supraventricular rhythm]] or a [[Junctional Tachycardias|junctional tachycardia]]. In tachycardias, this [[Media:narrow_tachycardia_flow.png|'''flowchart''']] will lead to the right diagnosis.<cite>ESCnarrowQRS</cite><br />
*If the QRS > 120ms it is either a [[Ventricular Arrhythmias|ventricular tachycardia]] or a [[Supraventricular Rhythms|supraventricular rhythm]] with additional [[Intraventricular Conduction|bundle branch block]]. This is a challenging difficulty in arrhythmia diagnosis, therefore a [[media:wideQRS_tachycardia_flow.png|'''flowchart''']] has been developed for this.<cite>brugada</cite><br />
<br />
==References==<br />
<biblio><br />
#ESCnarrowQRS pmid=14563598<br />
#Brugada pmid=2022022<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=QRS_Morphology&diff=5614
QRS Morphology
2007-12-26T05:13:54Z
<p>195.229.242.57: acgetd</p>
<hr />
<div>trgetr<br />
chiordomel<br />
{{nav|<br />
|previouspage=P_wave_morphology<br />
|previousname=Step 5: P wave morphology<br />
|nextpage=ST morphology<br />
|nextname=Step 7: ST morphology<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= <br />
}}<br />
<br />
The basic questions in judging QRS morphology are:<br />
*Are there any [[Q waves|pathological Q waves]] as a sign of previous myocardial infarction? <br />
*Are there signs of left or right ventricular [[hypertrophy]]? <br />
*Does the QRS complex show [[microvoltations]] (roughly QRS < 5mm)?<br />
*Is the conduction normal or [[Conduction delay|delayed]] (QRS-interval > 0,12s)? <br />
*Is the R wave propagation normal? Normally R waves become larger from V1-V5. At V5 it should be maximal. If the R wave in V2 is larger than in V3, this could be a sign of a (previous) [[Posterior MI|posterior myocardial infarction]]. Other causes are noted in the chapter [[Clockwise and Counterclockwise rotation]].<br />
<br />
If all these items are normal you can go on to the next step: [[ST morphology]].</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Conduction&diff=5602
Conduction
2007-12-25T23:07:01Z
<p>195.229.242.57: domdomeltdo</p>
<hr />
<div>acelerr<br />
{{nav|<br />
|previouspage=Rate<br />
|previousname=Step 2: Rate<br />
|nextpage=Heart axis<br />
|nextname=Step 4: Learn how to determine the heart axis<br />
}}<br />
<br />
[[Image:QRSwaves.jpg|thumb]]<br />
==The PQ interval==<br />
The PQ interval starts at the beginning of the atrial contraction and ends at the beginning of the ventricular contraction.<br />
[[Image:PR_interval_buildup.svg|thumb|The PR duration depends on the conduction velocity in the atria, AV node, His bundle, bundle branches and Purkinje fibers.]]<br />
<br />
<br />
The PQ interval (sometimes referred to as the PR interval as a Q wave is not always present) indicates how fast the action potential is transmitted through the AV node (atrioventricular) from the atria to the ventricles. Measurement should start at the beginning of the P wave to the beginning of the QRS segment.<br />
<br />
'''The normal PQ interval is between 0.12 and 0.20 seconds'''.<br />
<br />
A prolonged PQ interval is a sign of a degradation of the conduction system, increased vagal tone (Bezold-Jarisch reflex), or it can be pharmacologically induced. <br />
<br />
This is called [[Arrhythmias#Atrioventricular_block|1st, 2nd or 3rd degree AV block]].<br />
<br />
A short PQ interval can be seen in the [[Arrhythmias#WPW_syndrome|WPW syndrome]] in which a faster connection exists between the atria and the ventricles.<br />
{{clr}}<br />
<br />
==The QRS duration==<br />
The QRS duration indicates how fast the ventricles depolarize. <br />
<br />
The ventricles depolarize normally within 0.10 seconds. When this is longer than 0.12 seconds, this is a [[conduction delay| conduction delay]]. Possible causes of a QRS duration > 0.12 seconds include:<br />
* [[LBBB|Left bundle branch block]]<br />
* [[RBBB|Right bundle branch block]]<br />
* [[Electrolyte Disorders]]<br />
* [[Idioventricular Rhythm|Idioventricular rhythm]] and [[Pacemaker|paced rhythm]]<br />
<br />
==The QT interval==<br />
The QT interval indicates how fast the ventricles are repolarized and how fast they are ready for a new heart cycle<br />
The normal value for QTc(orrected) is: 440-450ms for men and 450-470ms for women. <cite>Moss</cite><br />
<br />
[[Image:QRSinterval.jpg|thumb| The QT interval start at the onset of the Q wave and ends where the tangent line for the steepest part of the T wave intersects with the baseline of the ECG. Click on the image for a bigger image]]<br />
<br />
The QT interval comprises the QRS-complex, the ST-segment, and the T-wave.<br />
<br />
In a (serious) prolonged QT time, is takes longer for the myocardial cells to be ready for a new cardiac cycle. There is a possibility that some cells are not yet repolarized, but that a new cardiac cycle is already initiated. These cells are at risk for uncontrolled depolarization and induce a [[Arrhythmias#Torsade_de_pointes|torsade de pointes]], a ventricular tachycardia.<br />
<br />
The QT interval is defined as follows: <cite>Lepeschkin</cite> The time between the beginning of the Q until the point where the steepest tangent line from the end of the T-wave intersects with the base line of the ECG. <br />
<br />
The difficult part is that the QT interval gets shorter if the heart rate increases. This cab be solved by correcting the QT time for heart rate using the Bazett formula::<br />
<br />
[[Image:Formule_QTc.png]]<br />
<br />
''at an RR interval 1 second, the (heart frequency 60/min) QTc=QT''<br />
<br />
Using the QTc calculator on the right, the QTc is easy extractable.<br />
<br />
<flash>file=QTc.swf|width=300|height=200|quality=best|align=right|salign=R||bgcolor=#FFF5F5</flash><br />
<br />
On the modern ECG machines, the QTc is given. However, the machines are not always capable of recognizing the correct QT time. Therefore, it is important to check this manually..<br />
<br />
The following formula is indicative for normal values of QT time (uncorrected):<br />
<br />
[[Image:Formule_QTn_nl.png]]<br />
{{clr}}<br />
<br />
===Difficult QT intervals===<br />
In some examples of the QT interval it can be difficult to measure a correct QT time. We have made a separate chapter: [[Difficult_QT| Measurement of difficult QT intervals]].<br />
<br />
===Causes of a prolonged QT interval===<br />
*Medication (i.e. anti-arrhythmics, tricyclic antidepressants, phenothiazedes, for a complete list look on [http://www.torsades.org Torsades.org]<br />
*Inherited [[Long QT syndrome|long QT syndrome]] (LQTS)<br />
*Cerebral (subarachnoid haemorrhage, stroke, trauma)<br />
*Post infarct<br />
<br />
===Short QT syndrome===<br />
If QTc is < 340ms [[Short_QT_Syndrome|short QT syndrome]] can be considered.<br />
<br />
== References ==<br />
<biblio><br />
#bazett Bazett HC. ''An analysis of the time-relations of electrocardiograms''. Heart 1920;7:353-370.<br />
#Lepeschkin pmid=14954534<br />
#Gaita pmid=12925462<br />
#Moss pmid=8256751<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Myocardial_Infarction&diff=5601
Myocardial Infarction
2007-12-25T23:06:11Z
<p>195.229.242.57: boctarel</p>
<hr />
<div>vitrocrol<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|supervisor= <br />
}}<br />
Ischemia occurs when part of the heartmuscle, the myocardium, is deprived form oxygen and nutrients. <br />
Common causes of ischemia are:<br />
* Narrowing or obstruction of a coronary artery.<br />
* A rapid arrhythmia, causing a disbalance in supply and demand of energy. <br />
<br />
A short period of ischemia causes ''reversibele'' effects: The heartcells will be able to recover. When the ep[isode of ischemia lasts for a longer period of time, heartmuscle cells will die. This is called a '''heart attack''' or '''myocardial infarction'''. That is why it is critical to recognize ischemia on the ECG in an early stage. <br />
<br />
Severe ischemia will reuslts in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment. <br />
<br />
'''Signs and symptoms of myocardial ischemia:'''<br />
* Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower jaw or the left arm<br />
* Fear of dying <br />
* Nausea<br />
* Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock <br />
* Rhythm dysturbances (in particular increasing prevalnce of ventricular ectopia, ventricular tachycardia, AV block)<br />
<br />
===Risk assessment of Cardiovascular disease===<br />
The narrowing of the coronary artery leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or stroke, can be estimated using [http://www.escardio.org/initiatives/prevention/prevention-tools/SCORE-Risk-Charts.htm SCORE system] which is developed by the European Society of cardiology (ESC). <br />
As shown in the figure, the most important risk factors for myocardial infarction are:<br />
*Male sexe<br />
*Smoking<br />
*Hypertension<br />
*Diabetes Mellitus<br />
*Hypercholesterolemia<br />
<br />
===Risk assessment of ischemia===<br />
An [[Exercise Testing|exercise test]] such as a bicycle or treadmilltest, may be usefull in detecting myocardial ischemia after exercise.<cite>accexercise</cite> In such a test, a continuous ECG registration is performed during exercise. The ST-segment, blood pressure asnd clinical status of the patient (i.e. chest complaints) are monitorered during and after the test.<br />
<br />
An [[Exercise Testing|exercise test]] is positive for myocardial ischemia when the following criteria are met: <br />
* Horizontal or downsloping ST-depression of > 1mm, 60 or 80ms after the J-point<br />
* ST elevation of > 1.0 mm<br />
{{clr}}<br />
<br />
==Diagnosis of myocardial infarction==<br />
[[Image:Stelevatie_en.png|thumb|ST elevation is measured 60ms or 80ms after the J point]]<br />
<br />
The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial infarction is defined as:<cite>Alpert</cite><br />
<br />
* Elevated blood levels of cardiac enzymes ([[w:Creatine_kinase|CKMB]] or [[w:Troponin|Troponin T]]) AND <br />
* One of the following criteria are met:<br />
** The patient has typical complaints<br />
** The ECG shows ST elevation or depression<br />
** [[Pathologic_Q_Waves|pathological Q waves]] develop on the ECG<br />
** A coronary intervention had been performed (such as stent placement)<br />
<br />
So detection of elevated serum heartenzymes is more important than ECG changes. However, the heartenzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So especially in the first few hours after the myocardial infarction the ECG can be crucial.<br />
<br />
;Significant ST elevation is defined as:<br />
:ST elevation of more than 2mm in two chest leads or more than 1 mm in two adjacent limb leads<br />
:ST elevation is measured 60ms or 80ms after the J-point<br />
<br />
A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).<cite>martin</cite><br />
<br />
Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but is explained in these seperate chapters:<br />
*[[MI Diagnosis in LBBB]]<br />
*[[MI Diagnosis in RBBB]]<br />
*[[MI Dagnosis in Paced Rhythm]]<br />
{{clr}}<br />
<br />
==The location of the infarct==<br />
[[Image:coronary_anatomy.png|thumb| An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.]]<br />
[[Image:lead_overview.png|thumb|Overview of the seperate ECG leads. The lead with ST elevation 'highlights' the infarct. An infarction of the inferior wall will result in ST elevation in leads II, III and AVF. A lateral wall infarct results in ST elevation in leads I and AVL. An Anterior wall infarct results in ST-elevation in the precordial leads.]]<br />
[[Image:MI_colours_en.png|The coloured figure shows contiguous leads in matching colours|thumb]]<br />
[[Image:MIregions.jpg|thumb|The ST elevation points at the infarct location. Inferior MI = ST elevation in red regions (lead II,III and AVF). Lateral MI = ST elevation in blue leads (lead I, AVL, V5-V6). Anterio MI: ST elevation in yellow region (V1-V4). Left main stenosis: ST elevation in gray area (AVR) ]]<br />
The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an '''anterior wall infarction''' is different than those of an '''inferior wall infarction'''. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.<br />
<br />
The heart is supplied of oxygen and nutrients by the right and left coronary arteries. The left coronray artery (the '''Left Main''' or LM) divides itself in the '''left anterior descending''' artery (LAD) and the '''ramus circumflexus''' (RCX). The '''right coronary artery''' (RCA) connects to the ramus descendens posterior (RDP). With 20% of the normal population the RDP is supplied by the RCX. This called '''left dominance'''.<br />
<br />
Below you can find several different types of myocardial infarcation. Click on the specific infarct location to see examples.<br />
<br />
<br />
{| class="wikitable"<br />
|- <br />
|+'''Help with the localisation of a myocardial infarct'''<br />
|-<br />
!localisation<br />
!ST elevation<br />
!Reciproke ST depression<br />
!coronary artery<br />
|-<br />
| [[Anterior MI]] <br />
| V1-V6<br />
| None<br />
| LAD<br />
|-<br />
| [[Septal MI]]<br />
| V1-V4, disappearance of septum Q in leads V5,V6<br />
| none<br />
| LAD<br />
|-<br />
| [[Lateral MI]]<br />
| I, aVL, V5, V6<br />
| II,III, aVF<br />
| RCX or MO<br />
|-<br />
| [[Inferior MI]]<br />
| II, III, aVF<br />
| I, aVL<br />
| RCA (80%) or RCX (20%)<br />
|-<br />
| [[Posterior MI]]<br />
| V7, V8, V9<br />
| high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view)<br />
| RCX<br />
|-<br />
| [[Right Ventricle MI]]<br />
| V1, V4R<br />
| I, aVL<br />
| RCA<br />
|-<br />
| [[Atrial MI]]<br />
| PTa in I,V5,V6<br />
| PTa in I,II, or III<br />
| RCA<br />
|-<br />
|}<br />
{{clr}}<br />
<br />
The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report, the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.<cite>AHACAG</cite><br />
<br />
==Development of the ECG during persistent ischemia==<br />
[[Image:AMI_evolutie.png|thumb| The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave]]<br />
[[Image:PathoQ.png|thumb| A [[Pathologic_Q_Waves|pathological Q wave]]]]<br />
[[Image:anteriorMInegativeT.png|thumb| Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated.<cite>Novotny</cite><cite>Jensen</cite><cite>Chevalier</cite>]]<br />
The cardiomyocytes in the ''subendocardial'' layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction ''transmural ischemia'' develops. <br />
<br />
In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, '''large peaked T waves''' (or ''hyperacute'' T waves), then '''ST elevation''', then'''negative T waves''' and finally '''[[Pathologic_Q_Waves|pathologic Q waves]]''' develop.<br />
<br />
{| class="wikitable"<br />
|- <br />
|+'''Evolution of the ECG during a myocardial infarct'''<br />
|-<br />
!<br />
!see figure<br />
!change<br />
|-<br />
!minutes<br />
| not in figure<br />
b<br />
| hyperacute T waves (peaked T waves)<br />
ST-elevation<br />
|-<br />
!hours<br />
| c<br />
d<br />
| ST-elevation, with terminal negative T wave<br />
negative T wave (these can last for months)<br />
|-<br />
!days<br />
| e<br />
| [[Pathologic_Q_Waves|Pathologic Q Waves]]<br />
|-<br />
|}<br />
<br />
{{clr}}<br />
<br />
==References==<br />
<biblio><br />
#Wung pmid=16777513<br />
#martin pmid=17825710<br />
#Alpert pmid=10987628<br />
#accexercise pmid=12356646 <br />
#Menown pmid=10653675<br />
#LBTB pmid=11265742<br />
#AHACAG pmid=1116248<br />
#Novotny pmid=18019666<br />
#Chevalier pmid=12716101<br />
#Jensen pmid=15851335<br />
</biblio><br />
<br />
==External Links==<br />
A good introduction to [http://www.askdrwiki.com/mediawiki/index.php?title=Coronary_Angiography coronary angiography]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=AV_Conduction&diff=5600
AV Conduction
2007-12-25T23:05:18Z
<p>195.229.242.57: rolrolazelou</p>
<hr />
<div>varall<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt]]<br />
|supervisor= <br />
}}<br />
[[Image:AV_block_sequence.png|thumb|Sequence of AV block from incomplete to complete]]<br />
Conduction disturbances can occur at the level of the sinoatrial (SA) node, the atrioventricular (AV) node and the bundle branch system. <br />
In atrioventricular block the conduction between atria and ventricles is disturbed leading to an incread [[Conduction#PQ interval|PQ interval]] or to drop out of QRS complexes: atrial activity that is not followed by ventricular activity. Three degrees of block can be distinguished.<br />
<br />
==First degree AV block==<br />
[[Image:Rhythm_1stAVblock.png|thumb| 1st degree AV block. Although the PQ interval is prolonged all p-waves are followed by QRS complexes: there is no dropout of beats]]<br />
In first degree AV block there is a prolongation of PQ duration (PQ time > 0.20 sec). Still every p-wave is being followed by a QRS complex.<br />
First degree AV block is present in 16% of >90-year olds <cite>kelley</cite> and is mostly caused by a degeneration of the conduction system. First degree AV block is relatively harmless.<br />
{{clr}}<br />
==Second degree AV block==<br />
In second degree AV block not all p-waves are being followed by QRS complexes: beat dropout occurs. Second degree AV block can be categorized in 3 types:<br />
===Second degree AV block type I (Wenckebach)===<br />
[[Image:Wenckebach.png|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
[[Image:Wenckebach2.png|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
[[Image:Wenckebach3.jpg|thumb|Example of type I second degree AV block (Wenckebach)]]<br />
In second degree AV block type I, the PQ interval prolongs from beat to beat up until the drop-out of one QRS complex. The characteristics of a Wenkebach block:<br />
* QRS complexes cluster (e.g. a 5:4 block or 4:3 block)<br />
* The PQ interval prolongs every consecutive beat<br />
* The PQ interval that follows upon a dropped beat is the shortes.<br />
* The RR interval shortens (!) every consecutive beat.<br />
* The amount of block decreases during exercise (e.g. a 4:3 block improves into a 6:5 block)<br />
The conduction disturbance in a type I block originates in the AV node. Isolated second degree AV block type I is relatively benign and not a pacemaker indication.<br />
{{clr}}<br />
<br />
===Second degree AV block type II (Mobitz)===<br />
[[Image:Rhythm_Mobitz.png|thumb| Second degree AV block type II (Mobitz)]]<br />
In second degree AV block type II, beats are dropped irregularly without PQ interval prolongation. As the drop out of beats is irregular, no clustering of QRS complexes can be seen as in second degree block type I. Second degree AV block type II marks the starting of trouble and is a class I pacemaker indication. <cite>CITATION</cite><br />
The cause of second degree AV block type II can be found distally from the AV node: in the HIS bundle or in the bundle branches or Purkinje fibers. <br />
<br />
An important differential diagnosis of second degree AV block type II is an [[Atrial Premature Complexes|premature atrial complex]] with compensatory pause. This diagnosis is much more common and harmless.<br />
{{clr}}<br />
<br />
===High grade AV block===<br />
High grade AV block is defined as two or more p-waves not followed by QRS complexes.<br />
<br />
==Third degree AV block==<br />
[[Image:Rhythm_3rdAVblock.png|thumb| 3rd degree AV block. AV dissociation is present: there is no relation between p-waves and the (nodal) QRS complexes.]]<br />
[[Image:Rhythm_totalAVblock.png|thumb| Short lasting total AV block (initiated by adenosine infusion). P-waves are present, but no QRS complexes follow]]<br />
Third degree AV block is synonymous to ''total block'': absence of atrioventricular conduction. The P-waves and QRS complexes have no temporal relationship, which is called to [[AV dissociation]].<br />
The ventricular rhythm can be [[Nodal Rhythm|nodal]], [[Idioventricular Rhythm|idioventricular]] or absent. Absent ventricular rhythm results in asystole and death.<br />
<br />
During third degree AV block the blood supply to the brain can insufficient, leading to loss of consciousness. [[w:Stokes-Adams_Attack|Adams Stokes (or Stokes-Adams) attacks]] (often misspelled as Adam Stokes) attacks arte attacks of syncope or pre-syncope in the setting of third degree AV block.<br />
{{clr}}<br />
==References==<br />
<biblio><br />
#kelley pmid=17126661<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Repolarization_(ST-T,U)_Abnormalities&diff=5599
Repolarization (ST-T,U) Abnormalities
2007-12-25T23:03:46Z
<p>195.229.242.57: boccorboc</p>
<hr />
<div>cnacacpasre<br />
{{ActiveDiscuss}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt]]<br />
|moderator= [[user:VdBilt|I.A.C. van der Bilt]]<br />
|supervisor=<br />
}}<br />
*[[Repolarization (ST-T,U) Abnormalities|Early repolarization (normal variant)]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Juvenile T waves (normal variant)]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Nonspecific abnormality, ST segment and/or T wave]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST and/or T wave suggests ischemia]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST suggests injury]]<br />
*[[Repolarization (ST-T,U) Abnormalities|ST suggests ventricular aneurysm]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Q-T interval prolonged]]<br />
*[[Repolarization (ST-T,U) Abnormalities|Prominent U waves]]<br />
*[[Cardiac Memory|Cardiac Memory]]*</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Sinus_Node_Rhythms_and_Arrhythmias&diff=5598
Sinus Node Rhythms and Arrhythmias
2007-12-25T23:01:51Z
<p>195.229.242.57: elttrdarl</p>
<hr />
<div>trdelpas<br />
{{nav|<br />
|previouspage=Basics<br />
|previousname=Basics<br />
|nextpage=Rate<br />
|nextname=Step 2: Heart Rate<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user: Vdbilt|I.A.C. van der Bilt]]<br />
|supervisor= <br />
}}<br />
==Normal heart rhythm==<br />
[[Image:conduction_system_en.png|thumb|The conduction system handles the spreading of an electrical signal through the heart. The normal sinus rhythm begins in the sinus node and goes via the AV node to the His bundle where it splits via the right and left bundle branch.]]<br />
[[Image:PQRS_origin_en.png|thumb| During normal sinus rhythm, every atrial contraction (P-wave) is followed by a ventricular contraction (QRS complex).]]<br />
[[Image:normalSR.jpg|thumb|Normal sinus rhythm with a positive P-wave in I, II and AVF, and a biphasic P-wave in V1.]]<br />
The normal heart rhythm is ''sinus rhythm''. That means that the rhythm has its origin in the sinus node, the heart's fastest physiological impulse generator.<br />
The sinus node (SA) is located in the upper part of the wall of the right atrium. When the sinus node generates an electrical impulse, first the cells of the right atrium depolarise, then the cells of the left atrium, the AV (atrioventricular) node follows and at last the ventricles are stimulated via the His bundle.<br />
<br />
With this knowledge it is quite simple to recognise normal sinus rhythm on the ECG.<br />
<br />
;Criteria for normal sinus rhythm (see also [[Basics]]):<br />
*A P wave (atrial contraction) precedes every QRS complex<br />
*The rhythm is regular, but varies slightly while breathing<br />
*The frequency ranges between 60 and 100 beats per minute<br />
*The P waves maximum height is 2.5 mm in II and/or III<br />
*The P wave is positive in I and II, and biphasic in V1<br />
<br />
These last two definitions will be discussed in the topic [[P wave morphology]].<br />
Heart rhythms which are not sinus rhythm are [[arrhythmias]]. <br />
<br />
==Sinus arrhythmias==<br />
Some variants of sinusrhythm exist:<br />
*[[Asystole]]<br />
*[[Sinustachycardia|Sinustachycardia (>100 beats per minute)]]<br />
*[[Sinusbradycardia|Sinusbradycardia (<50 beats per minute)]]<br />
*[[Sinusarrest|Sinus arrest or pause]]<br />
*[[Sino-atrial_exit_block|Sino-atrial exit block]]<br />
*[[Sick Sinus Syndrome]]<br />
<br />
If the heart rate exceeds 100 bpm, the [[Arrhythmias#Tachyarrhythmias|tachcyardia flow chart]] should be followed.<br />
{{clr}}<br />
==Examples==<br />
[[Image:Normaal ecg.jpg|thumb| An example of normal sinus rhythm.]]<br />
[[Image:Nsr.jpg|thumb| Another example of normal sinus rhythm.]]<br />
<br />
{{clr}}<br />
[[nl:Ritme]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=ECGpedia:General_disclaimer&diff=5597
ECGpedia:General disclaimer
2007-12-25T23:01:08Z
<p>195.229.242.57: relc4tbaso</p>
<hr />
<div>virelbo<br />
:We do our best to ascertain that all information on this site is correct and up-to-date. However, given the open structure of this site, we cannot guarantee that it is. The information provided here is for educational and informational purposes only and designed primarily for use by qualified physicians and other medical professionals. In no way should it be considered as offering medical advice.</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Frequently_Asked_Questions&diff=5594
Frequently Asked Questions
2007-12-25T22:59:27Z
<p>195.229.242.57: paszelt</p>
<hr />
<div>sitact<br />
;Can I use a certain image / animation / video / piece of text in a non-commercial presentation?<br />
:Yes, in most cases you can. There are however certain exceptions to this rule. Some images on ECGpedia were provided by book or journal publishers who gave us permission to use that image on this site. The descriptions of these images will read something like: "reproduced with permission from...". If you want to use such items, you will have to ask the entity that holds the copyright. All material that is made by or for the Cardionetworks foundation is available for use and basis for your presentation according to a [http://creativecommons.org/licenses/by-nc/3.0/nl/deed.en_GB Creative Commons Attribution Noncommercial Share-Alike] license. If you cut the ECGpedia logo from a certain image, you will have to state elsewhere in the presentation that you obtained the material from ECGpedia, e.g. "'''ECG courtesy of Dr. Koster and ECGpedia.org'''". We do appreciate it when you [http://www.cardionetworks.org/contactCN.php let us know] that if you have used content from ECGpedia, just to have an idea who our audience is. <br />
<br />
;Can I use a certain image / animation / video / piece of text in a commercial presentation?<br />
:In general yes, but not without asking. In general we will not object you using any of our material as long as you do not copy-paste the whole website on a CD and sell it for money :-)... Please [http://www.cardionetworks.org/contactCN.php e-mail us for permission].<br />
<br />
;How can I use a flash movie from your site in my powerpoint presentation?<br />
:Read [http://www.adobe.com/go/tn_18822 this document] by Adobe to learn how.<br />
<br />
;When do I know enough to say that I can confidently interprete ECGs?<br />
:Of course, there is no definite answer to this question. However, the American College of Cardiology has published a list of [[ACC list|abnormalities a professional should be able to recognize]]. It is advisable to go through this list at the end of the course in order to recognize areas that need your attention. Understanding every item on the list does not guarantee that you will make the right decisions in every clinical situation.<br />
<br />
;Who are the people behind ECGpedia?<br />
:ECGpedia is an initiative of [http://cardionetworks.org Cardionetworks.org] a non-profit foundation whose goals is to advance medical knowledge, especially in the field of cardiology. The main contributors are: [[user:Drj|Jonas S.S.G. de Jong MD]], cardiology resident, author and moderator; [[user:Vdbilt|I.A.C. van der Bilt, MD]], cardiology resident, author and moderator; [[user:Tymen|Tymen T. Keller MD, PhD]], cardiology resident, author and moderator; [[user:Pgpostema|Pieter G. Postema MD]], cardiology research fellow, author and moderator; [http://www.medischeillustraties.nl Rob Kreuger], medical illustrator, made most of the drawings; and [[user:Bart|Bart Duineveld]], medical student, helps with technical issues, animations and lay-out.<br />
<br />
;My own ECG shows an abnormality what should I do?<br />
:The information on this site should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. For questions like these we advise you to contact your physician.<br />
<br />
;Can I trust the information on your site?<br />
{{ECGpedia:General_disclaimer}}<br />
<br />
;Do you protect the privacy of the patients whose ECGs / images / cases are presented?<br />
{{ECGpedia:Privacy_policy}}<br />
<br />
;What is the financial source of this project?<br />
:The [http://cardionetworks.org Cardionetworks.org] foundation is a non-profit charity foundation. The content of all websites maintained by the cardionetworks foundation is not influenced by sponsors. As the foundation was only recently started, no outside sources of funding have been contacted and the foundation has been funded privately by the founders. Feel free to [http://www.cardionetworks.org/contactCN.php contact the foundation] if you would like to sponsor or have sponsorship suggestions. We do not allow any advertisements on our sites. We also do not allow sponsors to influence any contents.<br />
<br />
;How can I contact you?<br />
:Please contact the [http://www.cardionetworks.org/contactCN.php secretary of Cardionetworks] for any further questions.<br />
<br />
;How can I contribute content to ECGpedia?<br />
{{:Contribute to ECGpedia}}<br />
<br />
We subscribe to the [http://www.hon.ch/HONcode/Conduct.html?HONConduct571624 HONcode] principles of the Health On the Net Foundation. [[Image:HONConduct571624.jpg]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Basics&diff=5592
Basics
2007-12-25T22:58:06Z
<p>195.229.242.57: ricboerrice</p>
<hr />
<div>noormonn<br />
{{nav|<br />
|previouspage=Introduction<br />
|previousname=Introduction<br />
|nextpage=Rate<br />
|nextname=Step 1: Heart Rate<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|editor= <br />
}}<br />
==How do I begin to read an ECG?==<br />
[[Image:nsr.png|thumb| A short ECG registration of normal heart rhythm (sinus rhythm)]]<br />
[[Image:Normaal ecg.jpg|thumb| An example of a normal ECG. ''Click on the Image for an enlargement'']]<br />
<br />
Click on the ECG to see an enlargement.<br />
Where do you start when interpreting an ECG?<br />
* on the top left are the patient's information, name, sex and date of birth<br />
* at the right of that are below each other the [[Frequency]], the [[Conduction|conduction times]] (PQ,QRS,QT/QTc), and the [[heart axis]] (P-top axis, QRS axis and T-top axis)<br />
* further to the right is the interpretation of the ECG written (this often misses in a 'fresh' ECG, but later the interpretation of the cardiologist or computer will be added)<br />
* down left is the 'paper speed' (25 mm/s on the horizontal axis), the sensitivity (10mm/mV) and the filter's frequency (40Hz, filters noise from eg. lights)<br />
* finally there is a calibration on the ECG, on the beginning of every lead is a vertical block that shows with what amplitude a 1 mV signal is drawn. So the height and depth of these signals are a measurement for the voltage. If this is not the set at 10 mm, there is something wrong with the machine setting.<br />
* further we have the ECG leads themselves of course, these will be discussed below.<br />
<br />
Note that the lay-out is different for every machine, but most machines will show the information above somewhere.<br />
{{clr}}<br />
<br />
==What does the ECG register?==<br />
An ECG is a registration of the heart's electric activity.<br />
Just like skeletal muscles, the heart is electrically stimulated to contract. This stimulation is also called ''activation'' or ''excitation''. Cardiac muscles are electrically charged at rest. The inside of the cell is negatively charged relative to the outside (resting potential). If the cardiac muscle cells are electrically stimulated they depolarize (the resting potential changes from negative to positive) and contract.<br />
As the impulse spreads through the heart, the electric field changes continually in size and direction. The ECG is a graphical visualisation of these electric signals in the heart.<br />
<br />
==The ECG represents the sum of the action potentials of millions of cardiomyocytes==<br />
{| class="wikitable" align="right" width=385px font-size="70%"<br />
|- <br />
!<flash>file=Single_cardiomyocyte.swf|width=382|height=315|quality=best|align=right||</flash><br />
|-<br />
| This movie shows the contraction of a single (rabbit) heart cell. The glass electrode measures the electrical current in the heart cell (with the[[w:Patch_clamp|patch-clamp method]]). The electrical signal is written in blue and shows the actionpotential. ''Courtesy of Arie Verkerk and Antoni van Ginneken, AMC, Amsterdam, The Netherlands''.<br />
|-<br />
|}<br />
[[Image:Hart_cells_en.png|thumb|The heart consists of approximately 300 trillion cells]]<br />
[[Image:cells_in_rest_en.png|thumb|In rest the heart cells are negatively charged. Through the depolarization by surrounding cells they become positively charged and they contract.]]<br />
[[Image:Ion_currents_en.png|thumb|During the depolarization sodium-ions stream inwards the cell. Subsequently the calcium-ions stream into the cell. These calcium-ions give the actual muscular contraction. Finally the potassium-ions stream out of the cell. During the repolarisation the ion concentration is corrected. On the ECG, an action potential wave coming towards the electrode is shown as a positive (upwards) signal. Here the ECG electrode is represented as an eye.]]<br />
The individual [[action potential|action potentials]] of the individual cardiomyocytes are averaged. The final result which is shown on the ECG is actually the average of trillions of microscopic electronical signals.<br />
{{clr}}<br />
<br />
==The electric discharge of the heart==<br />
[[Image:conduction_system_en.png|thumb]]<br />
<flash>file=Normal_SR.swf|width=300|height=400|quality=best|align=right||</flash><br />
'''The sinal node (SA node) contains pacemakercells which determine the heart frequency.'''<br />
'''First the [[heart|atria]] depolarise and contract, after that the [[heart|ventricles]]'''<br />
The electrical signal between the atria and the ventricles goes from the sinus node, via the atria to the AV-node (atrioventricular transition) to the His bundle and subsequently to the right and left bundle branch, which end in a dense network of Purkinje fibers.<br />
{{clr}}<br />
<br />
==The different ECG waves==<br />
[[Image:PQRS_origin_en.png|thumb| The origin of the different waves on the ECG]]<br />
[[Image:Epi_endo_en.png|thumb| The QRS complex is formed by the sum of the electric avtivity of the inner (endocardial) and the outer (epicardial) cardiomyocytes]]<br />
[[Image:Qrs-shapes.png|thumb| Example of the different QRS configuations]] <br />
The [[P_wave_morphology|'''P wave''']] is the result of the atrial depolarization. This depolarization starts in the SA (sino-atrial) node. The signal produces by pacemakercells in the SA node is conducted by the conduction system to the right and left atria. Normal atrial repolarisation is not visible on the ECG (but can be visible during [[atrial infarction]] and [[pericarditis]]). <br />
<br />
The [[QRS_morphology|'''QRS complex''' ]] is the average of the depolarization waves of the inner (endocardial) and outer (epicardial) cardiomyocytes. As the endocardial cardiomyocytes depolarize slightly earlier than the outer layers, a typical QRS pattern occurs (figure). <br />
<br />
The [[ST_morphology|'''T wave''']] represents the repolarisation of the ventricles. There is no cardiac muscle activity during the T wave.<br />
<br />
One heart beat consists of an atrial depolarization --> atrial contraction --> p-wave, ventricular depolarization --> ventricular contraction --> ORS-complex and the resting phase (including the repolarization during the T-wave) between two heart beats.<br />
<br />
Have a look at this excellent [[http://www-medlib.med.utah.edu/kw/pharm/hyper_heart1.html animation of the heart cycle]]<br />
<br />
The origin of the '''U wave''' is unknown. This wave possibly results from "afterdepolarizations" of the ventricles.<br />
<br />
The letters "Q", "R" and "S" are used to describe the QRS complex:<br />
*Q: the first negative deflection after the p-wave. If the first deflection is not negative, the Q is absent.<br />
*R: the positive deflection<br />
*S: the negative deflection after the R-wave<br />
<br />
*small print letters (q, r, s) are used to describe deflections of small amplitude. For example: qRS = small q, tall R, deep S. <br />
*R`: is used to describe a second R-wave (as in a [[right bundlebranch block]])<br />
See figure for some examples of this.<br />
{{clr}}<br />
<br />
==The history of the ECG==<br />
[[Image:Einthoven.gif|thumb|[[w:Einthoven|Willem Einthoven (1860-1927), the founder of the current ECG]]]]<br />
[[Image:einthECG1.png|thumb|ECG from Eindhoven's first publication. ''Pfügers Archiv March 1895, page 101-123'']]<br />
[[Image:stringgalvanometer.jpg|thumb|Einthoven's string-galvanometer, now in the Science Museum in Londen. The patient had to put his hands in salt baths to which the electrodes were connected. ''Image from the [http://www.ieee.org/portal/cms_docs_iportals/iportals/aboutus/history_center/conferences/che2004/Landman.pdf IEEE history society]''.]]<br />
[[Image:modern_ecg.jpg|thumb|The last generation of ECG equipment. Image courtesy of [http://www.gehealthcare.com/euen/cardiology/ General Electric]]]<br />
The history of the ECG goes back more than one and a half century<br />
<br />
In '''1843''' Emil Du Bois-Reymond, a german physiologist, was the first to describe "action potentials" of muscular contraction. He used a highly sensitive galvanometer, which contained more than 5 km of wire. Du Bios Reymond named the different waves: "o" was the stable equilibrium and he was the first to use the p, q, r and s to describe the different waves. <cite>Dubois</cite> However, in his excellent paper on the 'Naming of the waves in the ECG' Dr Hurst credits Einthoven for being the first to use PQRS and T.<cite>Hurst</cite><br />
<br />
In '''1850''' M. Hoffa described how he could induce irregular contractions of the ventricles of doghearts by administering electrical shock. <cite>Hoffa</cite><br />
<br />
In '''1887''' the English physiologist Augustus D. Waller from Londen published the first human electrocardiogram. He used a capillar-electrometer. <cite>Waller</cite><br />
<br />
[[w:Einthoven|The dutchman Willem Einthoven]] (1860-1927) introduced in 1893 the term 'electrocardiogram'. He described in '''1895''' how he used a galvanometer to visualize the electrical activity of the heart. In 1924 he received the Nobelprize for his work on the ECG. He connected electrodes to a patienta showed the electrical difference between two electrodes on the galvanometer. We still now use the term: Einthovens'leads. The string galvanometer (see Image) was the first clinical instrument on the recording of an ECG.<br />
<br />
In 1905 Einthoven recorded the first 'telecardiogram' from the hospital to his laboratoy 1.5 km away.<br />
<br />
In 1906 Einthoven published the first article in which he described a series of abnormal ECGs: left- and right bundlebranchblock, left- and right atrialdilatation, the U wave, notching of the QRS complex, ventricular extrasystoles, bigemini, atrialflutter and total AV block. <cite>Einthoven</cite><br />
{{clr}}<br />
<br />
==The ECG electrodes==<br />
[[Image:ECGelectrodes.jpg|thumb|click on the Image for an enlargement]]<br />
Electric activity going through the heart, can be measured by external (skin)electrodes. The electrocardiogram (ECG) registers these activities from these electrodes which have been attached on diffrent places on the body. In total, twelve leads are calculated using ten electrodes.<br />
<br />
The ten electrodes are:<br />
* '''the extremity electrodes:'''<br />
** LA - left arm<br />
** RA - right arm<br />
** N - neutral, on the right leg (= electrisch aarde of nulpunt ten opzichte waarvan de electrische spanning wordt gemeten)<br />
** F - foot, on the left leg<br />
It makes no difference whether the electrodes are attached proximal or distal on the extremities. ''However'', it is best to be uniform in this. (eg. do not attach an electrode on the left shoulder and one on the right wrist).<br />
<br />
* '''the chest electrodes:'''<br />
** V1 - placed in the 4th intercostal space, right of the sternum<br />
** V2 - placed in the 4th intercostal space, left of the sternum<br />
** V3 - placed between V2 and V4<br />
** V4 - placed 5th intercostal space in the nippleline. Official recommendations are to place V4 under the breast in women.<cite>Kligfield</cite><br />
** V5 - placed between V4 and V6 <br />
** V6 - placed in the midaxillary line on the same height as V4 (horizontal line from V4, so not necessarily in the 5th intercostal space)<br />
<br />
{{clr}}<br />
<br />
Using these 10 electrodes, 12 leads can be derived. There are 6 extremity leads and 6 precordial leads.<br />
===The Extremity Leads===<br />
[[Image:ECGafleidingen.jpg|thumb]]<br />
The extremity leads are:<br />
<br />
*'''I''' from the right to the left arm<br />
*'''II''' from the right arm to the left leg<br />
*'''III''' from the left arm to the left leg<br />
An easy rule to remember: lead '''I''' + lead '''III''' = lead '''II'''<br />
This is done with the use of the height or depth, independent of the wave (QRS, P of T).<br />
Example: if in lead I, the QrS complex is 3 mm in height and in lead III 9mm, the height of the QRS-complex in lead II is 12mm.<br />
<br />
Other extremity leads are:<br />
<br />
*'''AVL''' points to the left arm<br />
*'''AVR''' points to the right arm <br />
*'''AVF''' points to the feet<br />
<br />
The capital A stands for "augmented" and V for "voltage".<br />
<br />
(aVR + aVL + aVF = 0)<br />
{{clr}}<br />
<br />
===The Chest Leads===<br />
The precordial, or chestleads, '''(V1,V2,V3,V4,V5 and V6)''' 'observe' the depolarization wave in the frontal plane<br />
<br />
''Example'': V1 is close to the right ventricle and the right atrium. Signals in these areas of the heart have the largest signal in this lead. V6 is the closest to the lateral wall of the left ventricle.<br />
<br />
===Special Leads===<br />
In case of an inferior wall infarct, extra leads may be used:<br />
#In a right side ECG, V1 and V2 remain on the same place.V3 to V6 are placed on the same place but mirrored on the chest. So V4 is in the middle of the right clavicle. On the ECG it should be marked that it is a ''Right sided ECG''. V4R (V4 but right sided) is a sensitive lead to diagnose right ventricular infarction.<br />
#Leads V7-V8-V9 can be used to diagnose a posteriorinfarct. It is means that after V6, leads are pkaced towards the back. See the chapter[[Ischemia]] for other ways of diagnosing posterior infarction.<br />
<br />
{{:Technical Problems}}<br />
<br />
==References==<br />
<biblio><br />
#Dubois Du Bois-Reymond, E. ''Untersuchungen über thierische Elektricität''. Reimer, Berlin: 1848.<br />
#Hoffa Hoffa M, Ludwig C. 1850. ''Einige neue versuche uber herzbewegung''. Zeitschrift Rationelle Medizin, 9: 107-144<br />
#Waller Waller AD. ''A demonstration on man of electromotive changes accompanying the heart's beat.'' J Physiol (London) 1887;8:229-234<br />
#Einthoven Einthoven W. ''Le telecardiogramme''. Arch Int de Physiol 1906;4:132-164<br />
#Einthoven2 Einthoven W. ''Ãber die Form des menschlichen Electrocardiogramms''. Pfügers Archiv maart 1895, pagina 101-123<br />
#Marey Marey EJ. ''Des variations electriques des muscles et du couer en particulier etudies au moyen de l'electrometre de M Lippman.'' Compres Rendus Hebdomadaires des Seances de l'Acadamie des sciences 1876;82:975-977 <br />
#Marquez pmid=12177632<br />
#Hurst pmid=9799216<br />
#Kligfield pmid=17322457<br />
</biblio><br />
<br />
==External links==<br />
*[http://www.ecglibrary.com/ecghist.html An extensive history of the ECG]<br />
<br />
[[nl:Grondbeginselen]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Chamber_Hypertrophy_and_Enlargment&diff=5590
Chamber Hypertrophy and Enlargment
2007-12-25T22:55:03Z
<p>195.229.242.57: domolorolr</p>
<hr />
<div>oueltdar<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
In hypertrophy the heart muscle is thicker. This can have different causes. Left ventricular hypertrophy results from an increase in left ventricular workload, e.g. during hypertension or aortic valve stenosis. Right ventricular hypertrophy results from an increase in right ventricular workoad, e.g. emphysema or pulmonary embolisation. <br />
These causes are fundamentally different from [[Miscellaneous#Hypertrophic_Obstructive_Cardiomyopathy|hypertrophic obstructive cardiomyopathy (HCM)]], which is a congenital misallignment of cardiomyocytes resulting in hypertrophy. <br />
<br />
Left and right ventricular hypertrophy can be distinguished on the ECG:<br />
<br />
==Left ventricular hypertrophy==<br />
[[Image:E_lvh.jpg|thumb|LVH. R in V5 is 26mm, S in V1 in 15mm. The sum is 41 mm which is more than 35 mm and therefore LVH is present according to the Sokolow-Lyon criteria.]]<br />
[[Image:linker_ventrikel_hypertrofie.GIF|thumb]]<br />
<br />
As the left ventricular becomes thicker, the QRS complexes become larger. This is especially true for leads V1-V6. The S wave in V1 is deep, the R wave in V4 is high. Often some ST depression can be seen in leads V5-V6, which is in this setting is called a 'strain pattern'.<br />
<br />
To diagnose left ventricular hypertrhophy on the ECG one of the following criteria should be met:<br />
*R in V5 or V6 + S in V1 >35 mm. (this is called the '''Sokolow-Lyon criterium'''<cite>Sokolow</cite>)<br />
*R >26 mm in V5 or V6; <br />
*R >20 mm in I, II or III; <br />
*R >12 mm in aVL (in the absence of [[Conduction delay#LAFB|left anterior fascicular block]]);<br />
<br />
The '''Cornell-criterium''' has different values in men and women:<br />
* R in aVL and S in V3 >28 mm in men<br />
* R in aVL and S in V3 >20 mm in women<br />
<br />
Left ventricular hypertrophy has prognostic consequences as has been found in several studies.<cite>Levy</cite><cite>Sundstrom</cite><br />
<br />
===Examples===<br />
<gallery><br />
Image:LVH.jpg|ECG of patient with left ventricular hypertrophy according to the Sokolow-Lyon criteria<br />
Image:Extreme_lvh2.jpg|Another example of extreme left ventricular hypertrophy in a patient with severe aortic valve stenosis.<br />
Image:extreme_lvh.jpg|ECG of a patient with LVH and subendocardial ischemia leading to positive cardiovascular markers in blood testing.<br />
</gallery><br />
{{clr}}<br />
<br />
==Right ventricular hypertrophy==<br />
[[Image:Rechter_ventrikel_hypertrofie.GIF|thumb]]<br />
[[Image:E_rvh.jpg|thumb|Right ventricular hypertrohpy, the R wave is greater than the S wave in V1]]<br />
Right ventricular hypertrophy occurs mainly in lung disease or in congenital heart disease. <br />
The ECG shows a negative QRS complex in I (and thus a right [[heart axis]]) and a positive QRS complex in V1.<br />
<br />
*R > S in V1 (R must be > 0.5 mV) <br />
*Right [[heart axis]]<br />
{{clr}}<br />
<br />
==Left atrial enlargement==<br />
;Criteria for left atrial voor left atrial enlargement. Either<br />
:P wave with a broad (>0,04 sec or 1 small square) and deeply negative (>1 mm) terminal part in V1<br />
:P wave duration >0,12 sec in laeds I and / or II<br />
[[Image:left_atrial_enlargement.jpg|thumb| Left atrial enlargement]]<br />
[[Image:LAE_2.png|thumb| Left atrial enlargement with ECG.]]<br />
[[Image:ECG_LAtrD_v1.jpg|thumb| Left atrial enlargement as seen in lead V1.]]<br />
Left atrial enlargement is often seen in mitral valve insufficiency, resulting in backflow of blood from the left ventricle to the left atrium and subsequent incresed local pressure. <br />
{{clr}}<br />
<br />
==Right atrial enlargement==<br />
;Right atrial enlargement is defined as either:<br />
:P >2,5 mm in II / III and / or aVF <br />
:P >1,5 mm in V1.<br />
[[Image:right_atrial_enlargement.jpg|thumb| Right atrial enlargement]]<br />
[[Image:Rae.png|thumb| Right atrial enlargement]]<br />
Right atrial enlargement can result from increased pressure in the pulmonary artery, e.g. after pulmonary embolisation. A positive part of the biphasic p-wave in lead V1 larger than the negative part indicates right atrial enlargement. The width of the p wave does not change. <br />
{{clr}}<br />
<br />
==Biatrial enlargement==<br />
;Biatrial enlargement<br />
:Biphasic p wave in V1 of more than 0.04 sec duration. The positive initial part is > 1.5mm and the negative terminal part > 1mm<br />
In biatrial enlargement is the ECG whos signs of both left and right atrial enlargement. In V1 the p wave has large peaks first in positive and later in negative direction.<br />
<br />
==References==<br />
<biblio><br />
#Sokolow Sokolow M, Lyon TP: ''The ventricular complex in left verntricular hypterfophy as obtained by unipolar precordial and limb leads.'' Am Heart J 37: 161, 1949<br />
#Levy pmid=11352882<br />
#Sundstrom pmid=7923663<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Pacemaker&diff=5589
Pacemaker
2007-12-25T22:54:12Z
<p>195.229.242.57: erletod</p>
<hr />
<div>erreltarelm<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
[[Image:picture_pacemaker.jpg|thumb|A (used) DDDr pacemaker]]<br />
[[Image:paced2.gif|thumb| Ventricular paced rhythm shows ventricular pacemaker spikes]]<br />
[[Image:Pacemaker2.jpg |thumb| VVI pacemaker rhythm. Note the LBBB morphology with left axis deviation indicating the pacing lead in the right ventricular apex.]]<br />
<br />
<br />
A pacemaker is indicated when the electrical impulse conduction or formation is dangerously disturbed. The paced '''pacemaker rhythm''' can easily be recognized on the ECG as it shows '''pacemaker spikes''': vertical signals that represent the electrical activity of the pacemaker.<br />
<br />
In the first example image, the atria are being paced, but not the ventricles, resulting in a '''atrial paced rhythm'''. Accordingly the ventricular beat is delayed until the atrial signal has passed the AV node. In the second image the ventricles are paced directly, resulting in '''ventricular paced rhythm'''. As ventricular pacing occurs exclusively in the right ventricle the ECG shows a left bundle branch pattern. An exception to this rule is left ventricular pacing in patients with congenital anomalies and patients with an epicardial pacemaker that has been placed during surgery.<br />
<br />
===Pacemaker Coding===<br />
Pacemakers can be categorized according to the NASPE coding system, that usually consists of 3-5 letters. <br />
* The first letter represents the chamber where the signal is "sensed": O=none, A=atria, V=ventricle, D=dual (atrial and / or ventricle)<br />
* The second letter represents the chamber that is being paced: A=atria, V=ventricle, D=dual (atria and / or ventricle)<br />
* The third letter represents the action that follows the sensed signal: O = none, T = triggered, I = inhibited (i.e. if the heart beats by itself, the pacemaker is silent) and D = dual (T + I). <br />
* The fourth letter denotes whether the pacemaker has a fixed rate (0 = none) or has rate modulation (R).<br />
* The fifth letter indicates whether the pacemaker can pace both the atria and right chamber. This letter is seldomly used.<br />
<br />
===Commonly Used Pacemakers===<br />
The most often used codes are:<br />
* '''AAI''': the atria are paced, when the intrinsic atrial rhythm falls below the pacemakers threshold<br />
* '''VVI''': the ventricles are paced, when the intrinsic ventricular rhythm falls below the pacemakers threshold<br />
* '''DDD''': the pacemaker records both the atrial and ventricular rate and can pace one of each chambers when needed.<br />
* '''DDDR''': as above, but the pacemaker has a sensor that records a demand for higher cardiac output and can adjust the heart rate accordingly.<br />
* Biventricular pacemakers ('''CRT-D'''): leads in both ventricles are present to synchronize contraction. This cardiac synchronization therapy can improve symptoms and survival in some heart failure patients. <br />
* '''[[ICD]]''' (Internal Cardioversion Device): this device can detect and treat [[Ventricular Tachycardia]] and [[Ventricular Fibrillation]]. Usually the first treatment is anti-tachy pacing (pacing at a rate +- 10% above the ventricular rate in ventricular tachycardia, which can convert the rhythm to sinus rhythm). If this is not effective an defibrillator shock is delivered, usually with 16-36 Joules of energy. ICDs can save lives in patients who have a high risk of ventricular arrhythmias. All ICDs have optional pacemaker activity to treat bradycardias. New biventricular ICDs have 3 leads: an atrial lead, a left ventricular lead and a right ventricular lead.<br />
<br />
===Pacemaker Indications===<br />
A full list of pacemaker indications can be read in the ESC guidelines on cardiac pacing <cite>Vardas</cite>. A selection of class I indications are: chronic symptomatic third- or second degree (Mobtiz I or II) atrioventricular block. Syncope with sinus node disease. Alternating bundle branch block. Persisting AV block after surgery.<br />
<br />
===ICD Indications===<br />
<br />
===Atrial-sensed ventricular-paced rhythm===<br />
===AV dual-paced rhythm===<br />
===Pacemaker Malfunction===<br />
to be filled in ...<br />
====Failure of appropriate capture, atrial====<br />
====Failure of appropriate capture, ventricular====<br />
====Failure of appropriate inhibition, atrial====<br />
====Failure of appropriate inhibition, ventricular====<br />
====Failure of appropriate pacemaker firing====<br />
====Retrograde atrial activation====<br />
====Pacemaker mediated tachycardia====<br />
<br />
==External Links==<br />
[http://www.hrsonline.org/swPositionStatementFiles/ps101036428.asp Heart Rhytm Society]<br />
<br />
<br />
==References==<br />
<biblio><br />
#Vardas pmid=17726042<br />
#Gregoratos pmid=12379588<br />
</biblio><br />
<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Supraventricular_Rhythms&diff=5588
Supraventricular Rhythms
2007-12-25T22:53:22Z
<p>195.229.242.57: cnasita</p>
<hr />
<div>acereltaceld<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
'''Supraventricular Rhythms originate from the atria. Examples of supraventricular rhythms are:'''<br />
*[[Sinustachycardia]]<br />
*[[Atrial Rhythm]]<br />
*[[Atrial Flutter]]<br />
*[[Atrial Fibrillation]]<br />
*[[Atrial Tachycardia]]<br />
*[[AVRT|Atrio-ventricular Reentry Tachycardia AVRT]]<br />
<br />
'''Supraventricular [[Ectopic Beats|ectopic beats]] can result in:'''<br />
*[[Atrial Premature Complexes]]<br />
*[[Wandering Pacemaker]]<br />
*[[AV-nodal complexes]]<br />
<br />
'''Also read:'''<br />
*Flowchart: [[Media:narrow_tachycardia_flow.png|Approach to the Narrow Complex Tachycardia]] Adapted from <cite>ESCnarrowQRS</cite>.<br />
*[[Introduction to Arrhythmias]]<br />
*[[Mechanisms of Arrhythmias]]<br />
*[[Sinus node rhythms and arrhythmias]]<br />
*[[Junctional Tachycardias]]<br />
*[[Ventricular Arrhythmias]]<br />
<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''An overview of supraventricular tachycardias'''<br />
|-<br />
!<br />
!regularity<br />
!atrial frequency<br />
!ventricular frequency<br />
!origin (SVT/VT)<br />
!p-wave<br />
!effect of adenosine<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Narrow complex (QRS<0.12)'''<br />
|-<br />
! [[Sinustachycardia]]<br />
| regular<br />
| 100-180 bpm<br />
| 100-180 bpm<br />
| sinusnode (SVT)<br />
| precedes every QRS complex<br />
| gradual slowing<br />
|-<br />
! [[Atrial Fibrillation]]<br />
| grossly irregular<br />
| 400-600 bpm <br />
| 75-175 bpm <br />
| atria (SVT)<br />
| absent<br />
| slows down rate; irregularity remains<br />
|-<br />
! [[Atrial Flutter]]<br />
| regular (sometimes alternating block) <br />
| 250-350 bpm <br />
| 75-150 bpm (3:1 or 2:1 block is most common) <br />
| atria (SVT)<br />
| negative sawtooth in lead II <br />
| temporary reduced conduction (e.g. 4:1)<br />
|-<br />
! [[AVNRT]] <br />
| regular <br />
| 180-250 bpm<br />
| 180-250 bpm <br />
| AV-node (SVT)<br />
| in QRS complex (R') <br />
| stops<br />
|-<br />
! [[Atrial Tachycardia]]<br />
| regular<br />
| 120-250 bpm <br />
| 75-200 bpm<br />
| atria<br />
| precedes QRS, p wave differs from sinus-p <br />
| temporary AV-block<br />
|-<br />
! [[AVRT|Atrio-Ventricular Reentry Tachycardia (AVRT)- orthodromic]]<br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circle: av-node - ventricles - bypass - atria<br />
| RP < PR <br />
| stops<br />
|-<br />
! [[AVJT|AV junctional tachycardia]]<br />
| regular <br />
| 60-100 bpm<br />
| 70-130 bpm<br />
| AV node<br />
| RP < PR <br />
| reduces rate<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Wide complex (QRS>0.12)'''<br />
|-<br />
! [[Supraventricular tachycardia with block]]<br />
| (ir)regular depending on SVT<br />
| 150-250 bpm<br />
| 75-200 bpm<br />
| atria (SVT)<br />
| absent<br />
| temporary increased AV-block (eg 4:1)<br />
|-<br />
! [[AVRT|Atrio-ventricular Reentry Tachycardia (AVRT) - antidrome]]<br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circular: bypass - atria - av-node - ventricles<br />
| RP < PR <br />
| stops<br />
|-<br />
|}<br />
<br />
==References==<br />
<biblio><br />
#ESCnarrowQRS pmid=14563598<br />
</biblio></div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Introduction&diff=5587
Introduction
2007-12-25T22:51:37Z
<p>195.229.242.57: mongetro</p>
<hr />
<div>noaceleltl<br />
{{nav|<br />
|previouspage=/<br />
|previousname=/<br />
|nextpage=Basics<br />
|nextname=Basics<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= <br />
}}<br />
[[Image:nsr.png|thumb| A short ECG registration of normal heart rhythm (sinus rhythm)]]<br />
The aim of this course is to understand and recognize the normal ECG and to be able to interprete abnormalities. The course is divided in two different sections. First the [[basics]] will be presented. This is followed by the interpretation of the normal ECG according to the 7+2 step plan:<br />
* Step 1: [[Rhythm]]<br />
* Step 2: [[Rate]]<br />
* Step 3: [[Conduction]] (PQ,QRS,QT)<br />
* Step 4: [[Heart axis]]<br />
* Step 5: [[P wave morphology]]<br />
* Step 6: [[QRS morphology]]<br />
* Step 7: [[ST morphology]]<br />
* Step 7+1: [[Compare_the_old_and_new_ECG|Compare the current ECG with a previous one]]<br />
* Step 7+2: [[Conclusion]]<br />
<br />
<br />
Finally the real world is presented through [[Cases and Examples|practice ECGs]].<br />
<br />
If you have finished the course you are invited to come back to read more about abnormal ECGs in the ECG textbook.<br />
<br />
Also read our [[Frequently Asked Questions]] section.<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Rate&diff=5586
Rate
2007-12-25T22:51:01Z
<p>195.229.242.57: elc4talcnael</p>
<hr />
<div>alrolcole<br />
{{nav|<br />
|previouspage=Rhythm<br />
|previousname=Step 1: Rhythm<br />
|nextpage=Conduction<br />
|nextname=Step 3:Conduction intervals (PQ, QRS, QT, QTc)<br />
}}<br />
==What is the heart rate?==<br />
[[Image:ECGpapier.png|thumb| The width of a square on the ECG represents time]]<br />
[[Image:Ecgfreq.png|thumb| The countmethod to determine the heartfrequency. The second QRS-complex is between ''75'' and ''60'' beat per minute. This heartbeat is between that, around 65 beats per minute.]]<br />
<br />
To anwer this question, determine the time between two QRS complexes. Previously, the ECG was registered on a paperstrip transported through an ECG writer at the speed of 25 mm/second. Nowadays, digital ECG registration is common however, the method of determining the frequency remains the same. The ECG paper has a grid with thick lines 5 mm apart (= 0,20 second) and thin lines 1 mm (0,04 second). <br />
<br />
<br />
'''There are three simple methods to determine the heart rate (HR):'''<br />
# Count the small (1mm) squares between two QRS-complexes. Hense, the ECG paper runs with 25 mm/sec through the ECG writer, therefore:&nbsp;&nbsp;&nbsp;[[Image:HFformule_en.png]]This method works well in case of tachycardia (>100 beats/minute)<br><br />
# To determine the frequency of a normal sinus ritme: Use the sequence 300-150-100-75-60-50-43-37. Count from the first QRS complex, the first thick line is 300, the next line 150 etc. Stop the sequence at the next QRS complex. When the second QRS complex is in between two lines, take the mean of the two numbers from the sequence or use the finetune method listed to the right.<br />
# Non regular rhytms are best determined with the "3 second marker method" Count the number of QRS-complexes that fit in 3 seconds (some ECG writers register this period on the ECG paper). Multiply this number by 20 and find the number of beats/minute. <br />
{{clr}}<br />
{| class="wikitable" font-size="90%" align="right" <br />
|+'''The 'square counting' method can be finetuned with the following sequence'''<br />
|-<br />
|'''300'''||250||214||187||167||'''150'''||136||125||115||107||'''100'''||94||88||83||79||'''75'''||71||68||65||62||'''60'''<br />
|-<br />
|}<br />
{{clr}}<br />
<br />
==What changes the frequency of the heart?==<br />
A number of factors change the heart frequency including:<br />
* the (para) sympathic nerve system. <br />
** The '''sympathic system''' e.g. epinephrin (=adrenalin) increases the atrioventricular conduction and contractility. (the ''fight, fright, flight'' reaction)<br />
** The parasympathic system (nervus vagus) e.g. acetycholin decreases the frequency and atrioventricular conduction. The parasympathic system effects mainly the atria.<br />
* Cardiac filling increases the frequency.</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=QRS_axis&diff=5585
QRS axis
2007-12-25T22:50:27Z
<p>195.229.242.57: deltaa</p>
<hr />
<div>boctroccn<br />
{{nav|<br />
|previouspage=Conduction<br />
|previousname=Step 3: Conduction (PQ, QRS, QT, QTc)<br />
|nextpage=P_wave_morphology<br />
|nextname=Step 5: P wave morphology<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor= <br />
}}<br />
<br />
==What is the electrical heartaxis?==<br />
[[Image:hartas2.jpg|thumb|The heartaxis indicates the average direction of the depolarization wave. A normal heartaxis, the picture shows an example, is between -30 and +90 degrees. In this example, the heartaxis is +45 degrees.]]<br />
[[Image:einthhartas.png|thumb|Heartaxis from the original publication of Einthoven. Reprinted from The Lancet, March 30 1912, Einthoven W.,<br />
''The Different Forms of The Human Electrocardiogram and Their Signification'', 853-861, 1912, with permission from<br />
Elsevier]]<br />
The electrical heartaxis is an average of all depolarizations in the heart. The depolarization wave begins in the right atrium and proceeds to the left and right ventricle. Because the left ventricle wall is thicker than the right wall, the arrow indicating the direction of the depolarization wave is directed to the left.<br />
<br />
For a lot of people, this is a difficult concept. The theoretic part seems difficult but by doing it a lot, it will become clear.<br />
{{clr}}<br />
<br />
==How do you determine the electrical heartaxis==<br />
[[Image:hart_axis.png|thumb]]<br />
[[Image:hartasroset.png|thumb]]<br />
<br />
When you average all electrical signals from the heart, you can indicate the direction of the average electrical depolarization with an arrow (vector). This is the heartaxis. Especially a change of the heartaxis or an extreme deviation can be an indication for pathology.<br />
<br />
<i>For example:</i><br />
<br />
*Biggest QRS deflection in lead I: the electrical activity is directed to the left (of the patient)<br />
*Biggest QRS deflection in lead AVF: the electrical activity is directed down.<br />
<br />
This indicates a normal heartaxis. Usually, these two leads are enough to diagnose a normal heartaxis!<br />
<br />
The biggest vector in the heart is from the AV-node in the direction of the ventricular depolarization. Under normal circumstances, this is directed left and down.(towards leads I and AVF). The position of the QRS vector is given in degrees. See the figure, the middle of the figure is the AV-node. A horizontal line towards the left arm is defined as 0 degrees.<br />
<br />
A normal heartaxis is between -30 and +90 degrees.<br />
<br />
'''Rule:''' biggest QRS deflection in I and II is an intermediate = normal heartaxis. <br />
So positive deflections in I and II indicates a normal heartaxis.<br />
<br />
{{clr}}<br />
====Interpretation====<br />
The interpretation of the electrical heartaxis has a few rules of thumb:<br />
<br />
* First, when a positive depolarization wave moves towards a positive electrode, a positive, upwards deflection is registered on the ECG.<br />
*Second, there are 4 quadrants where the QRS-vector can point to:<br />
**left upper quadrant --> left axis deviation (between -30º and -90º)<br />
**left lower quadrant --> normal (between -30º and 90º)<br />
**right below and right --> right axis deviation (between 90º and -150º)<br />
**right upper quadrant --> extreme axis (between -90º and -150º)<br />
<br />
''Example'': <br />
<br />
The QRS in lead I, will have a negative deflection in a right axis deviation. The vector is not directed towards the electrode. However, lead AVF will be positive, the vector is directed towards the electrode.<br />
<br />
====Heart-axis Simulator====<br />
<br />
To understand how the ECG changes in axis deviations, this excellent axis-simulator may be helpful: http://www.blaufuss.org/ECGviewer/indexFrame2.html<br />
<br />
====Iso-electrical====<br />
'''Note:''' When the depolarization is perpendicular on the lead, this is called <br />
'''iso-electrical'''. The QRS is neither positive nor negative. <br />
<br />
====Undetermined axis ====<br />
When all extremity leads are biphasic, the axis is directed to the front or back, in a transverse plane. The axis is than '''undetermined'''.<br />
<br />
==Abnormal heartaxis==<br />
[[Image:left_axis_dev.jpg|thumb| Heartaxis deviation to the left in case of an inferior infarct. Left anterior hemi Block is a common cause. A left axis is between -30 and -90 degrees. The axis is -30 degrees.]]<br />
[[Image:right_axis_dev.jpg|thumb| Heartaxis deviation to the right in right ventricular load, as in COPD or pulmonary embolism. A right axis is between +90 and +180 degrees. In this case the axis is +135 degrees]]<br />
The direction of the vector can changes under different circumstances:<br />
<br />
#When the heart itself is rotated (right ventricular overload), obviously the axis turns with it. <br />
#In case of ventricular hypertrophy, the axis will deviate by the bigger electrical activity and the vector will turn towards the hypertrophied tissue. <br />
#Infarcted tissue is electrically dead. No electrical activity is registered and the QRS vector turns away from the infracted tissue<br />
#In conduction problems, the axis deviates too. When the right ventricle depolarizes later than the left ventricle, the axis will turn to the right (RBBB). This is because the right ventricle will begin the contraction later and therefore will also finish later. In a normal situation the vector is influenced by the left ventricle but now only by the right ventricle.<br />
<br />
{{clr}}<br />
<br />
==Examples of a left heartaxis==<br />
[[Image:LHA.png|thumb| Left heartaxis]]<br />
[[Image:LAHB.png|thumb| Left anterior hemi block]]<br />
*[[Conduction delay#LAFB| left anterior fascicular block]]<br />
*[[Ischemia#Inferior|Inferior myocardial infarction]]<br />
*[[Hypertrophy|Left ventricular hypertrophy]]<br />
*Pacemaker rhythm<br />
{{clr}}<br />
<br />
== Examples of a right heartaxis ==<br />
[[Image:rightaxis.jpg|thumb| Right heartaxis]]<br />
*[[Hypertrophy| Right ventricular hypertrophy]]<br />
*Right ventricular load, for example [[Pulmonary_Embolism|Pulmonary Embolism]] or Cor Pulmonale (as in COPD)<br />
*Atriumseptumdefect, ventricleseptumdefect<br />
{{clr}}<br />
<br />
==Microvoltages==<br />
{{:Microvoltages}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Technical_Problems&diff=5584
Technical Problems
2007-12-25T22:49:38Z
<p>195.229.242.57: montadelri</p>
<hr />
<div>cnaouoloalou<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de Jong]]<br />
|supervisor= <br />
}}<br />
==Lead reversals==<br />
[[Image:cableReversal1.png|thumb|Right and left arm lead reversal can be distinguished from the (much rarer) dextrocardia by looking at the precordial R wave progression.]]<br />
[[Image:cableReversal2.png|thumb|Right arm and left leg lead reversal. Lead II now measures the signal between the left and right leg, which is remote from the heart.]]<br />
Sometimes an ECG is made properly. Mistakes do happen and leads can be switched. Always remain careful to check this or you might come to the wrong conclusions. One of the most common mistakes is to switch the right and left arm. This will result in negative complexes in I, indicating a right axis deviation!<br />
<br />
Common mistakes are reversal of:<br />
*right leg and right arm:<br />
**Hardly any signal in lead II.<br />
*right and left arm electrodes; <br />
**reversal of leads II and III<br />
**reversal of leads aVR and aVL<br />
*left arm and left leg:<br />
**reversal of leads I and II<br />
**reversal of leads aVR and aVF<br />
**inversion of lead III<br />
*right arm and left leg:<br />
**inversion of leads I, II and III<br />
**reversal of leads aVR and aVF<br />
<br />
<br />
It is possible to distinguish lead reversal and [[w:Dextrocardia|dextrocardia]] by watching the precordial leads. Dextrocardia will show an R wave inversion, wheras lead reversal will not.<br />
{{clr}}<br />
<br />
==Artefacts==<br />
[[Image:Noise_move.png|thumb| Movement artefacts]]<br />
[[Image:ECG_Parkinson.png|thumb| Increasing movement artefacts in a Parkinson patient. The patient was in sinus rhythm! (which doesn't show on this short recording)]]<br />
[[Image:BaselineDrift.png|thumb| Baseline drift. The amplifier in the ECG machine has to re-find the 'mean'. This often occurs right after lead connection and after electric cardioversion.]]<br />
[[Image:cardioversion_from_afib.jpg|thumb| Cardioversion from atrial fibrillation to sinusrhythm, with clear baseline drift.]]<br />
[[Image:electric_noise_ecg.png|thumb| Electrical interference from a nearby electrical appliance. A typical example is a 100 Hz background distortion from fluorescent lights. Not to be confused with [[arrhythmias#atrial fibrillation|atrial fibrillation]].]]<br />
[[Image:electric_noise_ecg2.jpg|thumb| Another example of an artefact caused by an electrical appliance. The patients rhythm is regular. This strip shows 10 QRS complexes.]]<br />
<br />
Artefacts (disturbances) can have many causes. Common causes are:<br />
*Movement <br />
*Electrical interference<br />
<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Electrolyte_Disorders&diff=5583
Electrolyte Disorders
2007-12-25T22:48:55Z
<p>195.229.242.57: cocaelboli</p>
<hr />
<div>cnamondomcn<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[T.T. Keller]]<br />
|supervisor= <br />
}}<br />
===Hypercalcemia===<br />
Hypercalcemia results in a faster repolarization. Characteristics of hypercalcemia:<br />
*mild: broad based tall peaking T waves<br />
*severe: extremely wide QRS, low R wave, disappearance of p waves, tall peaking T waves.<br />
<br />
===Hypocalcemia===<br />
ECG-characteristics of hypocalcemia:<br />
*narrowing of the QRS complex<br />
*reduced PR interval<br />
*T wave flattening and inversion<br />
*prolongation of the QT-interval <br />
*prominent U-wave<br />
*prolonged ST and ST-depression<br />
<br />
===Hyperkalemia===<br />
[[Image:ecg_hyperkaliemie.jpg|thumb| Extreme hyperkalemia. No p-waves, wide QRS, tall peaking T waves.]]<br />
[[Image:ecg_hyperkaliemie2.jpg|thumb| Same patient after partial correction of the potassium level. Still no p-waves visible, wide QRS, tall peaking T waves.]]<br />
ECG characteristics of hyperkalemia:<br />
*Tall peaked T waves<br />
*Flattening p-waves. In extreme hyperkalemia p-waves may disappear altogether.<br />
*Prolonged depolarization leading to QRS widening (nonspecific intraventricular conduction defect) sometimes > 0.20 seconds<br />
<br />
At concentrations > 7.5 mmol/L atrial and [[Ventricular Fibrillation|ventricular fibrillation]] can occur.<br />
{{clr}}<br />
<br />
===Hypokalemia===<br />
[[Image:KJcasu18-3.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. ECG1]]<br />
[[Image:KJcasu18-2.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. ECG2]]<br />
[[Image:KJcasu18-1.jpg|thumb| Consecutive ECGs of a patient with hypokalemia. After correction of potassium levels.]]<br />
Hypokalemia is a low blood potassium level. This results in:<br />
*ST depression and flattening of the T wave<br />
*Negative T waves<br />
*A U-wave may be visible<br />
{{clr}}</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=QRS_Morphology&diff=5581
QRS Morphology
2007-12-25T22:47:58Z
<p>195.229.242.57: acelcoc</p>
<hr />
<div>chiordomel<br />
{{nav|<br />
|previouspage=P_wave_morphology<br />
|previousname=Step 5: P wave morphology<br />
|nextpage=ST morphology<br />
|nextname=Step 7: ST morphology<br />
}}<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|supervisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= <br />
}}<br />
<br />
The basic questions in judging QRS morphology are:<br />
*Are there any [[Q waves|pathological Q waves]] as a sign of previous myocardial infarction? <br />
*Are there signs of left or right ventricular [[hypertrophy]]? <br />
*Does the QRS complex show [[microvoltations]] (roughly QRS < 5mm)?<br />
*Is the conduction normal or [[Conduction delay|delayed]] (QRS-interval > 0,12s)? <br />
*Is the R wave propagation normal? Normally R waves become larger from V1-V5. At V5 it should be maximal. If the R wave in V2 is larger than in V3, this could be a sign of a (previous) [[Posterior MI|posterior myocardial infarction]]. Other causes are noted in the chapter [[Clockwise and Counterclockwise rotation]].<br />
<br />
If all these items are normal you can go on to the next step: [[ST morphology]].</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=ECGpedia:Privacy_policy&diff=5580
ECGpedia:Privacy policy
2007-12-25T22:47:24Z
<p>195.229.242.57: darc4tlicvic</p>
<hr />
<div>racbasl<br />
:All material on this site is checked so any information that could breech a patients privacy is removed in accordance to applicable Dutch laws.</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Ectopic_Complexes&diff=5579
Ectopic Complexes
2007-12-25T22:46:50Z
<p>195.229.242.57: vareltb</p>
<hr />
<div>olooloda<br />
{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
The pacemakercells in the sinusnode are not the only cells in the heart that can depolarize spontaneously. Actually all cardiomyoctyes have this capacity. The only reason why the sinusnode 'rules' is that it is the fastest pacemaker of the heart. From sinusnode to ventricle all healthy cardiomyocytes can function as a ectopic pacemaker. Ectopic pacemaker activity can originate from the atria (60-80 bpm), AV-node (40-60 bpm) and the ventricles (20-40 bpm). So, as the sinus rate drops (e.g. during atrial infarction), other cells can take over. The configuration of ectopic beats or extrasystoles, as seen on the ECG, reveals its origin, whether they are [[#Atrial premature beats|atrial]], nodal or [[#Premature ventricular beats(PVB) / Venticular extrasystoles (VES)|ventrical]].<br />
<br />
===Ectopic pacemakers===<br />
{| class="wikitable"<br />
|+ '''Heart cells with pacemaker activity'''<br />
! Celltype || Frequency || QRS width (*)<br />
|-<br />
| ''SA node'' (not ectopic)|| 60-100 bpm || narrow<br />
|-<br />
| ''Atrial || 55-60 bpm || narrow<br />
|-<br />
| ''AV Nodal ectopic pacemaker'' || 45-50 bpm || narrow<br />
|-<br />
| ''His bundle'' || 40-45 bpm || narrow<br />
|-<br />
| ''Bundle branch'' || 40-45 bpm || narrow or wide<br />
|-<br />
| ''Purkinje cells'' || 35-40 bpm|| wide<br />
|-<br />
| ''Myocardial cells'' || 30-35 bpm|| wide<br />
|-<br />
|}<br />
(*) QRS width can only be narrow if the conduction system downstream is normal (i.e. no bundle branch block)<br />
<br />
===Examples===<br />
*[[Atrial Rhythm]]<br />
*[[Wandering Pacemaker]]<br />
*[[Atrial Premature Complexes]]<br />
*[[AV-nodal complexes]]<br />
*[[Ventricular Premature Beats]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Rhythm_Puzzles&diff=5578
Rhythm Puzzles
2007-12-25T22:46:01Z
<p>195.229.242.57: erracouvart</p>
<hr />
<div>bastrocchira<br />
These Rhythm Puzzles have been published in the '''Netherlands Heart Journal''' and are reproduced here with permission from the publisher, '''Bohn Stafleu Van Loghum'''.<br />
==2007==<br />
# [[Wide complexes intervening regular sinus rhythm - 2]]<br />
# [[Palpitations after a MAZE procedure]]<br />
# [[Abnormal repolarisation, spot diagnosis]]?<br />
# [[An irregular rhythm at older age]]<br />
# [[Palpitations all the time]]<br />
# [[Five years of palpitations]]<br />
==2006==<br />
# [[Right you are]]<br />
# [[Should I be worried?]]<br />
# [[A pre-excited wide QRS complex: is that all there is?]]<br />
# [[An old lady with chest pain]]<br />
# [[Palpitations and dizziness in a 65-year-old-man]]<br />
# [[A narrow QRS complex tachycardia sensitive to Isoptin]]<br />
# [[And what about the ECG?]]<br />
# [[Palpitations again, have a closer look]]<br />
# [[Wide complexes intervening regular sinus rhythm]]<br />
==2005==<br />
# [[ECG puzzle: Appearances can be deceiving]]<br />
# [[Where do the extras come from?]]<br />
# [['The turtle and the hare']]<br />
# [[Now you see it, now you don't]] (answer is missing)<br />
# [[It's not what you think it is]]<br />
# [[One is enough, two is too many]]<br />
# [[The ECG of a (cardio)myopathy?]]<br />
# [[The ions have it]]<br />
<br />
==2004==<br />
# [[Puzzle 2004 2 73, A fainting lady with some extrasystoles|A fainting lady with some extrasystoles]]<br />
# [[Syncopated rhythm]]<br />
# [[Rhythm Puzzle: An irregular rhythm at older age|An irregular rhythm at older age]]<br />
# [[I think a niece of mine was referred to a neurologist]]<br />
# [[Just one Collaps During Soccer]]<br />
# [[Tachycardia terminated by adenosine]]<br />
# [[Nightly phenomena, day time work?]]</div>
195.229.242.57
https://en.ecgpedia.org/index.php?title=Cases_and_Examples&diff=5577
Cases and Examples
2007-12-25T22:45:17Z
<p>195.229.242.57: pasrelno</p>
<hr />
<div>racrolel<br />
Below you can find some common examples. ECGs can be magnified by clicking on the image....<br />
<br />
===Basic===<br />
Click on the name below the ECG for the case descriptions. Click on the ECG for enlargement of the ECG itself...<br />
<br />
<gallery caption:"Simple test ECGs"><br />
Image:Casus1_1.jpg|[[Example 1]]<br />
Image:Casus2_2.jpg|[[Example 2]]<br />
Image:KJcasus2.jpg|[[Example 3]]<br />
Image:KJcasus3.jpg|[[Example 4]]<br />
Image:KJcasus5.jpg|[[Example 5]]<br />
Image:KJcasus6.jpg|[[Example 6]]<br />
Image:KJcasus7.jpg|[[Example 7]]<br />
Image:KJcasus8.jpg|[[Example 8]]<br />
Image:KJcasus9.jpg|[[Example 9]]<br />
Image:KJcasus10.jpg|[[Example 10]]<br />
Image:KJcasus11.jpg|[[Example 11]]<br />
Image:KJcasus12.jpg|[[Example 12]]<br />
Image:KJcasus13.jpg|[[Example 13]]<br />
Image:KJcasus14.jpg|[[Example 14]]<br />
Image:KJcasus16.jpg|[[Example 15]]<br />
Image:KJcasu17-3.jpg|[[Example 16]]<br />
Image:KJcasu18-1.jpg|[[Example 17]]<br />
Image:triblock.png|[[Example 22]]<br />
Image:RVDB1.jpg|[[Example 23]]<br />
</gallery><br />
<br />
{{:Guess the Culprit}}<br />
<br />
===Contribute your ECG!===<br />
[mailto:ecgcursus@ecgpedia.org mail] or fax (faxnumber +31-84-755 0017) a typical or difficult ECG and we will add it to the site anonimized.</div>
195.229.242.57