Lecture 9 Flashcards
What can we use the ECG for?
We can use the ECG to predict diseases of the heart i.e. Wolf-Parkinson’s White Syndrome. you can tell from he ECG that there is an extra-bundle of tissue. The QRS starts early, there is a short PR interval, wide QRS, a delta wave (begging of QRS). Anybody with these signs have the potential of an arrhythmia.
What is a narrow-complex tachycardia?
The QRS is narrow. So the activation starts at the ventricles.
What is a wide-complex tachycardia?
The QRS is wide, but the activation starts at the atria. So activation is slower.
Describe long QT syndrome?
Represents the AP duration. If Ap is prolonged it can be a serious problem and generate arrhythmias. Most common way is drug induced, and genetic types (often relate to channels that aren’t functioning properly especially potassium channels). Because the potassium channels don’t work as properly, so the cell doesn’t repolarise as quickly and so the AP is prolonged. Sudden death events occurring out of the blue. You can end up with a ventricular tachycardia with abnormal twisting of the points.
What is a characteristic on the ECG of an AV block?
Where the PR interval is typically prolonged. Tells us there is something wrong with the AV node - may not or may lead to mechanical problems in the heart.
Describe RV Hypertrophy on an ECG?
The QRS complex is bigger than the normal one. Can see this via V1-V3 (where as V4-V6 are normal because that is LV).
Describe electrolyte disturbances?
So in Hyperkalaemia it is where potassium channels conduct more rapidly, leads to changes of the T wave. Where as Hypokalaemia, is where there is a fact T wave.
Describe Ischaemic Heart Disease (IHD)?
There is a range of changes and is variable depending on the person. Affects the T wave, will get QRS changes. Sequence of changes. The AP duration shortens, due to Na+/K+/ATPase has reduced, there is no energy. The potassium gradient has reduced, sodium inside the cell has reduced. Extracellularly there is high potassium. This will increase IKR current,a activate the current so it will depolarise earlier. This happens only in the ischaemic region. So there is heterogeneity - thus generates arrhythmias. First the T wave changes: tall peak T waves (mechanism around potassium handling - potassium leaking from damaged myocytes) - this an early sign of an infract. The ST segment changes (the first thing that a clinical sees) - there is current flow at the resting potential (the flat line is below the baseline - ischaemic zone has partially depolarised resting potential) during the plateau there is no current flow so the ST segment goes to the baseline (no current flow) thus it appears as ST segment elevation. Another possibility of ST segment elevation is that during the plateau the damaged cells do not get to a high AP as normal cells, thus there is current flow again which will raise or change the segment. The R wave decreases in height as well. Epicardial infarct - no activity - not as much tissue generating the dipoles. The electrodes facing the infarcted tissue will not have as great of QRS complex (positive component). Loss of R wave due to the tissue. If there is a transmural infarct, there will be no positive activity at all, thus there is just Q waves.
