Difference between revisions of "Clinical Disorders"

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* no delta wave
 
* no delta wave
 
==Left and right bundelbranch block==
 
==Left and right bundelbranch block==
See: [[Conductiondelay]]
+
See: [[Conduction_delay|Conduction delay]]
 
 
 
 
  
 
==References==
 
==References==

Revision as of 14:42, 6 May 2007

Medication

Digoxin

Typical for digoxin intoxication is the odd shaped ST-depression

ECG changes typical for digoxin intoxication (digoxin = Lanoxin) are:

  • odd shaped ST-depression.
  • T-wave flat, negative or biphasic
  • Short QT interval
  • Increased u-wave amplitude
  • Prolonged PR-interval
  • Brady-arrhytmias:
    • Sinusbradycardia
    • AV block. Including complete AV block and Wenkebach.
  • Tachyarrhythmias:
    • Junctional tachycardia
    • Atrialtachycardia
    • Ventricular ectopia, bigemini, monomorphic ventricular tachycardia, bidirectional ventricular tachycardia

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.

Anti-arhythmics

  • anti-arhythmics: These may lead to several ECG-changes;
    • broad and irregulair P-wave
    • broad QRS-complex
    • prolonged QT-interval (brady-, tachycardia, AV-block, ventricular tachycardia)
    • prominent U-wave
    • In case of intoxication, the above mentioned characteristics are more prominent

Additionally, several arrhtythmias can be seen.

Nortriptyline intoxication

An example of severe nortriptyline intoxication. The inhibitory effect of the sodiumchannel manifests as a broadened QRS complex and a prolonged QT interval.


Amitriptyline intoxication

An example of a severe amitriptylin intoxication. The inhibitory effect of the sodiumchannel manifests as a broadened QRS complex.
An ECG of the same patient before the intoxication.


Pericarditis

Several stages of pericarditis

Pericarditis is an inflammation of the pericardium. This can lead to ST elevation in all leads. Therefore, it is important to distinguish pericarditis from a myocardial infarction, which has more acute complaints and ST-elevations are limited to the infarct area.

In pericarditis four stages can be used:

  • stage I: ST elevation in all leads. PTa depression (depression between the end of the P-wave and the beginning of the QRS- complex)
  • stage II: pseudonormalisation (transition)
  • stage III: inverted T-waves
  • stage IV: normalisation

Keep into account that in stage I pericarditis, ST-elevation is present in all leads except in aVR, V1 and III.

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.

Acute peri/myocarditis causes aspecific ST changes. These can be accompanied with supraventricular and ventricular rhythmdisturbances and T-wave abnormalities.

Pulmonary embolism

In case of a pulmonary embolism several clinical features may be present:[1]

Pulmonary embolism cannot solely be diagnosed using an ECG, but it may be helpful.

COPD

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.

Pacemaker

See the chapter Pacemaker

Tamponade

In case of a tamponade, fluid collects in the pericardium. The pericardium is stiff and the heart cannot pump, because it cannot relax as well. The ECG shows:

  • Sinus tachycardia
  • Low-voltaged QRS complexes microvoltages
  • 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
  • PR segment depression (this can also be observed in an atrial infarction)

Ventricular Aneurysm

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).

Dilated Cardiomyopathy

Often, a LBBB or broadened QRS-complex can be seen. Additionally, aspecific ST changes are present with signs of left atrial enlargement.

Hypertrophic Obstructive Cardiomyopathy

A HOCM is an heditary illness. On the ECG there are signs of left ventricular hypertrophy and[P_top_morfologie|left atrial enlargement]].

Electrolyte disturbances

See chapter: electrolyte disturbances

Hypothermia

In hypothermia a number of specific chnages can be seen;

  • sinubradycardia
  • prolonged QTc-interval
  • ST-elevation (inferior and left precordial leads)
  • Osborne-waves (slow deflexions at the end of the QRS-complex)
An Osborne J wave


ECG changes after neurologic events

ECG of a 74 year old patient with a subarachnoid hemorrhage. Note the negative T-waves and the prolonged QT interval.

In 1938, Aschenbrenner [3] noted that repolarisation abnormalities may occur after increased intracranial pressure. Since then, many publications have occurred discribing ECG changes after acute neurological events.

De ECG changes that may occur are:

  • q-waves
  • ST-elevations,
  • ST-depressions,
  • T-wave changes. Large negative T waves over the precordial leads are observed frequently.
  • prolonged QT-interval.
  • prominent u-waves.

These abnormalites are frequently seen after subarachnoid_hemorrhage (SAH) (if measured serially, almost every SAH patients has at least one abnormal ECG.), but also in subdural haematoma, ischemic CVA's, brain Tumors, Guillain Barré, epilepsy and 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.

Contusio cordis / Commotio cordis

Contusio cordis is caused by a blunt trauma to the chest, often caused by a car- or motorbikeaccident or in martial arts[4]. Rhythmdisturbances may occur and even heartfailure. Diagnosis is made using echocardiography and laboratorytesting for cardiac enzymes. Possible ECG changes are:[5]

Not-specific changes

  • Pericarditis-like ST elevation or PTa depression
  • Prolonged QT interval

Myocardial damage

  • New Q waves
  • ST-T segment elevation or depression

Conduction delay

  • Right bundelbranchblok
  • Fascicular blok
  • AV delay(1st, 2nd, and 3rd degree AV blok)

Arrhythmias

  • Sinustachycardia
  • Atrial and ventricular extrasystoles
  • Atrial fibrillation
  • Ventricular tachycardia
  • Ventricular fibrillation
  • Sinusbradycardia
  • Atriala tachycardia

Lown Ganong Levine Syndrome

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:

  • short PR interval, < 120 ms
  • normal QRS complex
  • no delta wave

Left and right bundelbranch block

See: Conduction delay

References

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  1. Error fetching PMID 11018210: [Rodger]
  2. Error fetching PMID 9118684: [Ferrari]
  3. Aschenbrenner R, Bodechtel G, Über Ekg.-Veränderungen bei Hirntumorkranken. Journal of Molecular Medicine, 17, 9, 2/1/1938, Pages 298-302, http://dx.doi.org/10.1007/BF01778563

    [Aschenbrenner]
  4. Error fetching PMID 14681516: [Maron]
  5. Error fetching PMID 12695446: [Sybrandy]

All Medline abstracts: PubMed | HubMed