Lecture 8: ECG 2 Flashcards
Describe an ECG:
SAN (Not measurable, too small mass)
P wave = Atrial depolarisation
PR Segment = AV node, AV Bundle, Bundle branches
QRS: Ventricular depolarisation
Q -> Interventricular Septum (L->R depolarisation)
R -> Ventricular apex depolarisation
S -> Ventricular base depolarisation
ST: Isoelectric, plateau of ventricle AP
T wave: Ventricular repolarisation (assynchronous, thus long duration) (epi to endo direction)
Describe the deflection and and dipole relationship?
Depolarisation towards the positive dipole = positive deflection, away from positive = negative.
What are some problems with ECG?
Gross oversimplifications including but not limited to:
- The body is a volume conductor
- Varying conductivity
- Single dipole is not good representation of wavefront more detailed modelling uses multiple dipoles.
What is a basic guide to looking at ECG?
- Heart Rate (60-100)
- Rhythm
- Atrial Conduction (P Waves)
- Ventricular depolarisation
- Axis within norm. range
- Ventricular repolarisation
What are you looking at for rhythm?
Establishing whether this originates in atria or ventricles i.e P wave etc
i.e Normal sinus rhythm, can it be predicted or is it random
What are you looking at for atrial conduction?
P wave
- Usually positive lead 2, aVf, V2-6
- 3 small squares wide
What are you looking at for the PR interval?
Duration
- 3-5 small squares
- Consistency
What are you looking for in ventricle depolarisation?
- QRS shape / heights
- R wave should heighten from V1-5
- Q wave about 25% R wave height and negative
- QRS width (3 squares)
What do you look for in ventricular repolarisation?
- T wave is negative only in aVR and V1
- ST segment (isoelectric)
- QT segment = AP of cells and inversely proportional to HR. (abnormally prolonged increases risk of arrhythmias)
What is long QT syndrome?
A heart disease in which there is an abnormally long delay between excitation and repolarisation of the ventricles.
Usually the result of Na or K issues
What are common drug causes of long QT?
Anti-Arrhythmic drugs
What is long QT associated with?
- Syncope
- Arrhythmias (long QT abnormal refractoriness)
What else does ECG show?
1) Conduction issues
2) Heart (and lung) structure i.e hypertrophy
3) Electrolyte disturbances and drugs
4) IHD
How does hyperkalemia show?
- Some K channels conduct faster therefore faster repolarisation, more pronounced in epicardium, = Tall peaked T waves
How does hypokalemia show?
- Flat T waves
- Opposite effects of hyperkalemia
How does hypercalcemia show?
Increased Ca(o) leads to increased Ca(i) = inactivation of L type Ca channels, thus reduced Ca during plateau, thus reduced ADP, Shortens Ca plateau
How does hypocalcemia show?
- Opposite effect, prolonged ST segment
What can digitalis cause?
- ST segment depression
- T wave inversion (like ischemia)
- PR interval prolongation (1st degreee AV block)
Describe in an overview how the stages of MI change ECG:
- Ischemia (T wave)
- Injury (ST segment)
- Infarction (QRS complex)
Describe the sequence of events found in MI ECG changes:
- Tall peaked T waves (ONLY LEADS OVER DAMAGED AREAS)
- ST segment elevation (hours)
- reduced R wave amplitude (hours)
- T wave inversion (days)
- Pathological Q waves (days)
- ST segment returns to normal (days)
- T waves return to normal (weeks)
Pathological Q waves tend to be the only residual ECG signs of MI
How big must the ST segment shift be to be regarded as sig?
> 1mm
How does ST depression occur?
Current between two regions with different potentials
Describe the mechanism of how ischemia leads to altered ST shape:
Ischemia: Lowers RMP, Shortens AP, changes AP plateau
- Voltage gradient, current flow, measured / reflected by ST segment changes
Whats diastolic and systolic current of injury?
- Injury current occurs during diastole and is seen during ST
- Injury current occurs during plateau and is seen during ST (True ST)
What is the mechanism of MI changes to QRS?
Low R wave and Path Q waves;
Mechanism
- Electrical tissue electrically inactive (i.e electrical window through which the distant wall is recorded)
= Wavefronts coming towards overlying electrode are seen as reduced or absent
= wavefronts moving away from overlying electrode are emphasised
= Pathological Q waves (big)
= Reduced R waves
What doe leads opposite the infarct see?
Leads opposite infarct see inverse changes
- ST depression instead of elevation
- Tall T waves instead of inverted.
