ECG 2: Signs of Abnormality Flashcards Preview

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Flashcards in ECG 2: Signs of Abnormality Deck (27)
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What are the three signs on an ECG of WPW syndrome with a Wide complex QRS?

Why is this

Short PR
Wide QRS
Delta wave

Because its going don the slower conduction pathway


WPW and "Narrow complex Tachycardia"

Narrow QRS, and a re-entrant SVT


WPW syndrome is?

pre-excitation syndrome, which the ventricles of the heart are electrically activated earlier then normal through an 'accessory pathway' called the "Bundle of Kent".

Abnormal electrical pathway that doesn't have the delaying properties of the AV node


How can a ventricular Tachyarrhythmia occur?

Re-entry from atria to the ventricles.
-Rapid atrial rhythm where AV node cannot protect ventricles


How does WPW present?

-Most sufferers will remain asymptomatic throughout their entire lives
-episodes of unexplained syncope or palpitations
-small risk of sudden death


Treatment of WPW

removal of Bundle of Kent


Long QT Syndrome

Heart disease in with an abnormally long delay between ventricular depol -repolarization (delayed repolarisation). This reflects AP duration


Most common types of LQTS are?

Drug Induced: usually a result of anti-arrhythmic drugs like "amiodarone"

Genetic: due to mutation usually in ion channels. Usually prolong the Ventricular AP (APD)


Most Common type of Genetic LQTS?

Gene conducting slowed component of the K+ channel is mutated. This leads to an iKs abnormality as cells can't repolarise properly


How does Long QT Syndrome work?

Long QT > abnormal ventricular repolarisation > differences in the "refractoriness of myocytes > abnormal activation of the ventricles and thus arrhythmia


Complications of LQTS

Associated with Syncope and sudden death due to ventricular arrhythmias


Early after-depolarisations (EADs) can result in

-Continuously varying
-Torsade de Pointes - twisting of the points

May resolve spontaneously or progress to VF


During myocardial ischaemia what are some AP changes

All these changes are VARIABLE. All shorten ATP
-Na+/K+ ATPase reduced
-Transmemebrane K+ gradient reduced
-INa reduced
-Hyperkalemia(lots of K+ in the extracellular fluid) shortens AP duration (Increased [K+]o increases IKr)
-Activation of IKATP channels


Myocardial Infarction leads to a characteristic (though variable) and progressive ECG changes. These are

T wave changes
ST segment changes
QRS changes


T wave changes

1)Tall peaked T-waves due to K+ leaking from myocytes (same as hyperkalaemia)

-Not specific to MI
-Earliest signs of acute MI (so usually missed as you don't ECG till later)
- Localised to the leads facing area of injury
-5-30mins post-onset

2) Symmetrically inverted T-waves
-later (days)
-unknown mechanism


ST elevation

Usually earliest recognised sign of acute MI
Ischaemia; lowers resting membrane potential, shortens AP and changes AP plateu.

Leads to a voltage gradient between normal and ischaemic zones
-Injury current
-this is reflected by ST changes

2 theories: diastolic and systolic current of injury.


Diastolic Current of Injury

As the ischaemic zone has a partially depolarised resting potential, so the there is CURRENT FLOW at resting potential.
So instead of being at baseline (0) the ECG reads higher. Still reach the same plateau (baseline). So what APPEARS as ST elevation is actually still just reaching baseline

Apparent ST shift


Systolic Current of Injury

Injury occurs during AP plateau. Current flows during plateu when it should be isoelectric. True ST shift


"injury Current"

abnormal current flow either to/from normal to injured tissue


Loss of R wave height and pathological Q waves. (QRS changes)

As infarcted tissue is electrically inactive
-Wavefronts coming towards electrodes diminished or absent
-Wavefronts moving away from overlying electrode emphasized


Reciprocal changes

in leads 'opposite' those facing the infarct see inverse changes
-ST segment depression instead of elevation
-Tall T waves not inverted


How can we localise damage to areas of the heart

ECG changes only seen in areas overlying damage area.

Can also identify coronary arteries involved.


How does defibrillation work??

Evenly spreads the depolarisation, due to laminar structure this can occur



Some channels conduct faster when [K+] outside increases. Leads to faster repolarisation

-Tall peaked Twaves



Flat T waves



increase [Ca2+] outside leads to increased inside.
-Leads to inactivation of L-type Ca2+ channels
-reduces duration of Ca current during plateau
-Reduced APD, shorter QT interval



prolonged QT interval