L8: ECG2 Flashcards
what is a P-R interval and how long is it normally?
From start of P to start of QRS complex
~0.16 sec( 3-5 little squares)
what is the standard speed on ECG?
25 mm/s
Q-T interval
beginning of QRS to end of T-wave
S-T segment
from end of S to beginning of T
what does long Q-T mean?
problems with repolarisation
less time for filling
long Q-T syndrome
long Q-T syndrome
Long QT syndrome can be inherited or acquired. Inherited long QT syndrome is caused by genetic mutations that affect the ion channels responsible for the flow of potassium, sodium, and calcium ions across cardiac cell membranes. Acquired long QT syndrome can be triggered by certain medications, electrolyte imbalances (such as low potassium or magnesium levels), or underlying medical conditions.
Prolonged QT intervals can predispose individuals to a specific type of abnormal heart rhythm called torsades de pointes, which is characterized by a twisting pattern on an ECG. Torsades de pointes can cause rapid and irregular heartbeats, leading to fainting spells (syncope), seizures, or in severe cases, life-threatening ventricular arrhythmias, including ventricular fibrillation and sudden cardiac arrest.
Some individuals with long QT syndrome may experience symptoms such as palpitations, lightheadedness, fainting, or sudden cardiac arrest without any preceding symptoms.
EADs (early afterdepolarisations) can result in:
Continuously varying polymorphic VT
Torsade de Pointes – “twisting of the points”
may resolve spontaneously or progress to VF(ventricular fibrillation)
how can ECG be used in diagnosis. What does it tell us?
- Is conduction normal (e.g. PR interval, width of QRS)
- Is the morphology of the heart normal (height of QRS, axis)
- Are there signs of electrolyte disturbances
- Are there signs of ischemia/infarction (ST elevation/T
waves)
hypertrophy?
AV block
AV block:
-normal P-wave, occasionally normal QRS complex, but QRS does not always follow the P-wave. SA node is working, atria contracting. AV node failure( fibrous tissue, poor blood supply, isolated area), makes it vulnerable to hypoxia, also susceptible to becoming fibrotic.
1st degree AV block
takes a long time for the electrical
activity to pass through the AV node: long PR interval
2nd degree AV block
missing QRS complexes (see clinical
problem sessions)
3rd degree AV block
atria and ventricles contract independently
not a sinus rhythm, not generated by sinus node at all. AV node is not governed by SA node.
3rd degree AV block
atria and ventricles contract independently
not a sinus rhythm, not generated by sinus node at all. AV node is not governed by SA node.
how to identify hypertrophy on ECG
Need at least a 6 lead ECG- definitely more than just a rhythm strip to determine hypertrophy
Look at the height- the whole high from bottom to top of the signals(QRS)
*cannot have a negative R-wave. Always +ve.
Lead one is -ve( dominant deflection is -ve): signal is going the other way
Lead 3- most +ve
-> The heart is coming down to the right
Chest leads:
-V3: big +ve deflections. On the right side of heart
Big deflections on the right side of the heart-> right ventricular hypertrophy.
hyperkalaemia
Hyperkalemia refers to a higher-than-normal concentration of potassium in the bloodstream.
what ion disturbance leads to peaked T-waves
hyperkalaemia
- some K+ channels conduct faster when [K+] o increases
leading to faster repolarisation - effect more pronounced at epicardium (more [K+] o
sensitivity here) - leads to tall peaked T waves
what is the physiology behind S-T elevation
Cardiac AP changes in myocardial ischaemia
the infarcted/ ischaemiac area- smaller AP
resting membrane potential is closer to zero
Maximum depolarisation is not as +ve
Mostly because it is hypoxic> ATP-ase pumps cannot work so well, cannot maintain the Na+/K+ gradient within thew cell, which is very important. No gradient= K+ inside the cell lowers and Na+ leaks into the cell.
- Na+/K+ ATPase reduced
- Transmembrane potassium gradient reduced
- I Na reduced
- Hyperkalemia shortens AP duration (increased [K+ ] o increases IKr )
- Activation of I K,ATP channels (reduced [ATP] i ) shortens action potential duration
In the ischaemic regions – hence inhomogeneous electrical properties
may reentry
ST segment depression- Non-transmural ischemia
characteristics
If just a small area, not all the way through the wall- tends to be ischemic, reduced oxygen supply, hopefully repairable- resting membrane potential gets higher due to the leak of +ve charge.
Have AP- now the infarcted area and the normal area are both depolarised- equilises
ST segment elevation- Transmural ischemia
characteristics
If the infarct is all the way through(may be infarct, not just ischemia)- transmural- baseline potential is -ve, because the area is +ve relative to the surrounding and will be sending +ve charge away from the electrodes(towards the top of the heart)- shows as -ve of ECG.
During depolarisation- the same- isoelectric period
Baseline- back to -ve potential.
Even though looks like the problem is during the AP( AP lasting the whole time during depolarisation and repolarisation) the problem is actually at rest. But because at rest everything is the same at 0, do not pick it up until AP happens.
ST elevation tells us that we have an area of the heart closest to the recording electrode that is sitting at a +ve charge relative to the rest of the tissue. The infarcted area is effectively +ve- does not have the -ve membrane potential that its supposed to have.
!!RED ALARM-> need to quickly restore the oxygen to that part of the heart before death of the heart tissue.
Time course of ECG signs of MI
QRS- R-wave changes
