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 ion disturbance leads to flat T-waves
hypokalaemia
Hypokalemia, which is a decrease in the level of potassium in the bloodstream, can affect the electrical conduction system of the heart, leading to various changes in the electrocardiogram (ECG) waveform, including flattened T-waves.
The T-wave on the ECG represents the repolarization phase of the ventricles, where the electrical activity returns to its resting state. In hypokalemia, the reduced levels of potassium can disrupt the normal repolarization process, causing alterations in the shape and duration of the T-wave. Flattening of the T-wave is one of the characteristic ECG findings associated with hypokalemia.
ECG signs of MI and timing of events
MI- heart attack -ischemia of the heart-> cell death-> infarction
Infarction- total death of the cell
Signs of ischemia:
-peaked T-waves. Happen quickly. At this stage the cells are just hypoxic
-ST elevation ~ 30 min after the onset of feeling breathless and pain in the chest.
-Reduced R-wave
-Overtime things tend to correct themselves to the point when weeks later ECG can look normal. The only thing left: pathological Q-waves: Q wave is bigger than normal
what is the most important sign to see during MI on ECG? MUST SEE
S-T elevation
the gap between the QRS and T-wave is not isoelectric
has to be seen on 2 leads( 1 lead not enough)
at least 2 little squares above the baseline
what are the criteria for the diagnosis of anterior STEMI( ST elevation MI)?
Elevation of at least 2 mm in two
contiguous chest leads (V1-V6) is
needed for the diagnosis of anterior
STEMI (ST elevation MI)
has to be seen on 2 leads( 1 lead not enough)
at least 2 little squares above the baseline
vessel affected by ischemia on anteroseptal side of the heart. What leads show ST elevation?
V1-4
vessel affected by ischemia on anterior side of the heart. What leads show ST elevation?
V2-5
vessel affected by ischemia on anterolateral side of the heart. What leads show ST elevation?
V3-6
reciprocal change in ST. What is it?
if the ischemia is at the back of the heart, do not have leads there BUT can see ST DEPRESSION on the leads in the front
ST elevation timing
~30 min after onset of symptoms
goes away over time
Needs to be monitored
