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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> | |||
{{clr}} | |||
=== Nortriptyline Intoxication === | === Nortriptyline Intoxication === | ||
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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, spirochetes, auto-immune reactions, borreliosis (Lyme's disease) and HIV/AIDS. | [[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. | ||
{{clr}} | |||
==Pulmonary Embolism== | ==Pulmonary Embolism== | ||
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==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}} | ||
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* No delta wave | * No delta wave | ||
==Ebstein== | ==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. | 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. | ||
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#T wave inversion in V1-V4 and Q waves in V1-V4 and II, III and aVF. | #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> | #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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#hypoth pmid=2738372 | #hypoth pmid=2738372 | ||
#khairy pmid=18056539 | #khairy pmid=18056539 | ||
#schuller pmid=21615816 | |||
#bb pmid=10866327 | |||
</biblio> | </biblio> | ||
}} | }} | ||
[[Category:ECG Textbook]] | [[Category:ECG Textbook]] | ||