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Clinical Disorders: Difference between revisions
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===Digoxin=== | ===Digoxin=== | ||
[[Image:med_digitalis.png|thumb|300px|Typical for digoxin intoxication is the oddly shaped ST-depression]] | [[Image:med_digitalis.png|thumb|300px|Typical for digoxin intoxication is the oddly shaped ST-depression]] | ||
ECG changes typical for digoxin | ECG changes typical for digoxin '''use''' (digoxin = Lanoxin) are: | ||
*Oddly shaped ST-depression | *Oddly shaped ST-depression with 'scooped out' appearance of the ST segment (see figure) | ||
* | *Flat, negative or biphasic T wave | ||
*Short QT interval | *Short QT interval | ||
*Increased u-wave amplitude | *Increased u-wave amplitude | ||
*Prolonged PR-interval | *Prolonged PR-interval | ||
*Sinus bradycardia | |||
ECG changes typical for digoxin '''intoxication''' are: | |||
*Bradyarrhythmias: | *Bradyarrhythmias: | ||
**AV block. Including complete AV block and Wenkebach. | **AV block. Including complete AV block and Wenkebach. | ||
*Tachyarrhythmias: | *Tachyarrhythmias: | ||
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Intoxication can lead to an SA-block or AV-block, sometimes in combination with tachycardia. '''NB''' these effects are increased by hypokalemia. In extreme high concentrations rhythm disturbances (''ventricular tachycardia, ventricular fibrillation, atrial fibrillation'') may develop. | Intoxication can lead to an SA-block or AV-block, sometimes in combination with tachycardia. '''NB''' these effects are increased by hypokalemia. In extreme high concentrations rhythm disturbances (''ventricular tachycardia, ventricular fibrillation, atrial fibrillation'') may develop. | ||
{{clr}} | {{clr}} | ||
===Antiarrhythmics=== | ===Antiarrhythmics=== | ||
* '''Anti-arrhythmics:''' These may lead to several ECG-changes; | * '''Anti-arrhythmics:''' These may lead to several ECG-changes; | ||
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Additionally, several arrhthytmias can be seen. | Additionally, several arrhthytmias can be seen. | ||
===Beta blockers=== | |||
[[File:E000542.jpg|thumb|right|ECG of a patient with atenolol intoxication]]Beta blocker intoxication can result in bradycardia, hypotension, QRS widening and seizures. In a series of 260 patients with beta blocker intoxication, 41 (15%) developed cardiovascular morbidity and 4 (1.4%) died. Cardioactive coingestant (e.g. calcium channel blockers) was the only factor significantly associated with the development of cardiovascular morbidity. <cite>bb</cite> | |||
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=== Nortriptyline | === Nortriptyline Intoxication === | ||
<div align="center"> | <div align="center"> | ||
{| | {| | ||
| | | | ||
[[Image:ECG_nortr_intox.png|thumb|left|300px|An example of severe nortriptyline intoxication. The inhibitory effect | [[Image:ECG_nortr_intox.png|thumb|left|300px|An example of severe nortriptyline intoxication. The inhibitory effect on the sodium channel manifests as a broadened QRS complex and a prolonged QT interval.]] | ||
| | | | ||
[[Image:ECG_TCA_intox.jpg|thumb|left|300px| Another example of severe nortriptyline intoxication.]] | [[Image:ECG_TCA_intox.jpg|thumb|left|300px| Another example of severe nortriptyline intoxication.]] | ||
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|} | |} | ||
</div> | </div> | ||
=== Amitriptyline | === Amitriptyline Intoxication === | ||
<div align="center"> | <div align="center"> | ||
{| | {| | ||
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==Myocarditis== | ==Myocarditis== | ||
[[File:E000535.jpg|thumb|A patient with myocarditis and pericarditis showing diffuse ST elevation]] | |||
[[w:Myocarditis|Myocarditis]] is an inflammation of the myocardium and the interstitium. The symptoms are faint chest pain, abnormal heart rate and progressive heart failure. It can be caused by several factors: viruses, bacteria, fungi, parasites, | [[w:Myocarditis|Myocarditis]] is an inflammation of the myocardium and the interstitium. The symptoms are faint chest pain, abnormal heart rate and progressive heart failure. It can be caused by several factors: viruses, bacteria, fungi, parasites, spirochetes, auto-immune reactions, borreliosis (Lyme's disease) and HIV/AIDS. | ||
Acute peri/myocarditis causes nonspecific ST segment changes. These can be accompanied by supraventricular and ventricular rhythm disturbances and T-wave abnormalities. | Acute peri/myocarditis causes nonspecific ST segment changes. These can be accompanied by supraventricular and ventricular rhythm disturbances and T-wave abnormalities. | ||
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==Pulmonary | ==Pulmonary Embolism== | ||
See the chapter [[Pulmonary Embolism]] | See the chapter [[Pulmonary Embolism]] | ||
==Chronic | ==Chronic Pulmonary Disease Pattern== | ||
The ECG shows low voltage QRS complexes in leads I, II, and III and a right axis deviation. This is caused by the increased pressure on the right chamber. This leads to right ventricular hypertrophy. | [[File:E000004.jpg|thumb|right|An example of right ventricular hypertrophy (and right atrial enlargement) in a patient with chronic pulmonary hypertension due to peripheral embolisation.]]The ECG shows low voltage QRS complexes in leads I, II, and III and a right axis deviation. This is caused by the increased pressure on the right chamber. This leads to right ventricular hypertrophy. | ||
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==Pacemaker== | ==Pacemaker== | ||
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==Hypertrophic Obstructive Cardiomyopathy== | ==Hypertrophic Obstructive Cardiomyopathy== | ||
A HOCM is | A HOCM is a hereditary illness. | ||
On the ECG there are signs of [[hypertrophy|left ventricular hypertrophy]] and [[P wave morphology|left atrial enlargement]]. | On the ECG there are signs of [[hypertrophy|left ventricular hypertrophy]] and [[P wave morphology|left atrial enlargement]]. | ||
==Electrolyte | ==Electrolyte Disturbances== | ||
See chapter: [[electrolyte disturbances]] | See chapter: [[electrolyte disturbances]] | ||
==Hypothermia== | ==Hypothermia== | ||
[[Image:osborne.png|thumb|left|250px| An | [[Image:osborne.png|thumb|left|250px| An Osborn J wave]] | ||
[[Image:Osborn-wave.gif|thumb|left|250px|Osborn wave. 81-year-old black male with BP 80/62 and temperature 89.5 degrees F (31.94 C).]] | |||
<div style="float:right"> | <div style="float:right"> | ||
<gallery> | <gallery> | ||
Image:osborne_ecg.jpg|A 12 lead ECG of a patient with a body temperature of 32 degrees Celsius. Note the sinus bradycardia, the prolonged QT interval (QTc is not prolonged) and the | Image:osborne_ecg.jpg|A 12 lead ECG of a patient with a body temperature of 32 degrees Celsius. Note the sinus bradycardia, the prolonged QT interval (QTc is not prolonged) and the Osborn J wave, most prominently in leads V2-V5 | ||
Image:JJ0001.jpg|An ECG of a patient with a body temperature of 28 degrees Celsius. | Image:JJ0001.jpg|An ECG of a patient with a body temperature of 28 degrees Celsius. | ||
</gallery> | </gallery> | ||
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* Prolonged QTc-interval | * Prolonged QTc-interval | ||
* ST segment elevation (inferior and left precordial leads) | * ST segment elevation (inferior and left precordial leads) | ||
* | * Osborn-waves (slow deflections at the end of the QRS-complex) | ||
{{clr}} | {{clr}} | ||
==ECG | ==ECG Changes after Neurologic Events== | ||
[[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.]] | [[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.]] | ||
In 1938, Aschenbrenner <cite>Aschenbrenner</cite> noted that repolarization abnormalities may occur after increased intracranial pressure. Since then, many publications have described ECG changes after acute neurological events. | In 1938, Aschenbrenner <cite>Aschenbrenner</cite> noted that repolarization abnormalities may occur after increased intracranial pressure. Since then, many publications have described ECG changes after acute neurological events. | ||
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These abnormalities 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_hematoma|subdural hematoma]], 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 limited prognostic value. However, the ECG changes can be accompanied with myocardial damage and echocardiographic changes. The cause of the ECG changes is not yet clear. The most common hypothesis is that of a neurotramitter "catecholamine storm" caused by sympathetic stimulation. | These abnormalities 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_hematoma|subdural hematoma]], 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 limited prognostic value. However, the ECG changes can be accompanied with myocardial damage and echocardiographic changes. The cause of the ECG changes is not yet clear. The most common hypothesis is that of a neurotramitter "catecholamine storm" caused by sympathetic stimulation. | ||
==Cardiac | ==Cardiac Contusion== | ||
Cardiac contusion (in latin: contusio cordis or commotio cordis) is caused by a blunt trauma to the chest, often caused by a car or motorbike accident or in martial arts<cite>Maron</cite>. Rhythm disturbances and even heart failure can occur. Diagnosis is made using echocardiography and laboratory testing for cardiac enzymes. | Cardiac contusion (in latin: contusio cordis or commotio cordis) is caused by a blunt trauma to the chest, often caused by a car or motorbike accident or in martial arts<cite>Maron</cite>. Rhythm disturbances and even heart failure can occur. Diagnosis is made using echocardiography and laboratory testing for cardiac enzymes. | ||
Possible ECG changes are:<cite>Sybrandy</cite> | Possible ECG changes are:<cite>Sybrandy</cite> | ||
''' | '''Nonspecific changes''' | ||
*Pericarditis-like ST elevation or PTa depression | *Pericarditis-like ST elevation or PTa depression | ||
*Prolonged QT interval | *Prolonged QT interval | ||
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*ST-T segment elevation or depression | *ST-T segment elevation or depression | ||
'''Conduction delay''' | '''Conduction delay''' | ||
*Right | *Right bundle branch block | ||
*Fascicular blok | *Fascicular blok | ||
*AV delay(1st, 2nd, and 3rd degree AV blok) | *AV delay(1st, 2nd, and 3rd degree AV blok) | ||
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* Normal QRS complex | * Normal QRS complex | ||
* No delta wave | * No delta wave | ||
==Ebstein== | |||
[[File:E000403.jpg|thumb|300px|ECG from a patient with Ebstein's anomaly showing huge P waves and low amplitude QRS waves. RBBB and T wave inversion are not present on this ECG.]] | |||
In Ebstein anomaly the tricuspid valve is inserted more apically than normal. This yields a very large right atrium. About 50% of individuals with Ebstein's anomaly have evidence of Wolff-Parkinson-White syndrome, secondary to the atrialized right ventricular tissue. | |||
Other abnormalities that can be seen on the ECG include | |||
#signs of right atrial enlargement or tall and broad 'Himalayan' P waves, | |||
#first degree atrioventricular block manifesting as a prolonged PR-interval | |||
#low amplitude QRS complexes in the right precordial leads | |||
#atypical right bundle branch block | |||
#T wave inversion in V1-V4 and Q waves in V1-V4 and II, III and aVF. | |||
#Q waves in II, III, AVF. These Q waves are thought to reflect fibrotic thinning of the right ventricular free wall and/or septal fibrosis with coexisting left posterior hemiblock<cite>khairy</cite> | |||
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==Left and right bundle branch block== | ==Left and right bundle branch block== | ||
See: [[Conduction_delay|Conduction delay]] | See: [[Conduction_delay|Conduction delay]] | ||
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==Cocaine Intoxication== | ==Cocaine Intoxication== | ||
|<!--col1-->[[Image:JJ00001.jpg|200px]] | |<!--col1-->[[Image:JJ00001.jpg|200px]] | ||
==Sarcoidosis== | |||
In patients with proven pulmonary sarcoidosis ECG changes can be used as a marker of cardiac involvement. Presence of a fractionated QRS or a Bundle Branch Block increases the likelihood of cardiac involvement.<cite>schuller</cite> | |||
{{Box| | {{Box| | ||
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#Maron pmid=14681516 | #Maron pmid=14681516 | ||
#hypoth pmid=2738372 | #hypoth pmid=2738372 | ||
#khairy pmid=18056539 | |||
#schuller pmid=21615816 | |||
#bb pmid=10866327 | |||
</biblio> | </biblio> | ||
}} | }} | ||
[[Category:ECG Textbook]] | [[Category:ECG Textbook]] | ||