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Cardiovascular MBCHB2 > Lecture 8: ECG 2 > Flashcards

Lecture 8: ECG 2 Flashcards

1
Q

Describe an ECG:

A

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)

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2
Q

Describe the deflection and and dipole relationship?

A

Depolarisation towards the positive dipole = positive deflection, away from positive = negative.

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3
Q

What are some problems with ECG?

A

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.
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4
Q

What is a basic guide to looking at ECG?

A
  1. Heart Rate (60-100)
  2. Rhythm
  3. Atrial Conduction (P Waves)
  4. Ventricular depolarisation
  5. Axis within norm. range
  6. Ventricular repolarisation
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5
Q

What are you looking at for rhythm?

A

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

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6
Q

What are you looking at for atrial conduction?

A

P wave

  • Usually positive lead 2, aVf, V2-6
  • 3 small squares wide
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7
Q

What are you looking at for the PR interval?

A

Duration

  • 3-5 small squares
  • Consistency
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8
Q

What are you looking for in ventricle depolarisation?

A
  • QRS shape / heights
  • R wave should heighten from V1-5
  • Q wave about 25% R wave height and negative
  • QRS width (3 squares)
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9
Q

What do you look for in ventricular repolarisation?

A
  • 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)
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10
Q

What is long QT syndrome?

A

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

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11
Q

What are common drug causes of long QT?

A

Anti-Arrhythmic drugs

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12
Q

What is long QT associated with?

A
  • Syncope

- Arrhythmias (long QT abnormal refractoriness)

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13
Q

What else does ECG show?

A

1) Conduction issues
2) Heart (and lung) structure i.e hypertrophy
3) Electrolyte disturbances and drugs
4) IHD

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14
Q

How does hyperkalemia show?

A
  • Some K channels conduct faster therefore faster repolarisation, more pronounced in epicardium, = Tall peaked T waves
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15
Q

How does hypokalemia show?

A
  • Flat T waves

- Opposite effects of hyperkalemia

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16
Q

How does hypercalcemia show?

A

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

17
Q

How does hypocalcemia show?

A
  • Opposite effect, prolonged ST segment
18
Q

What can digitalis cause?

A
  • ST segment depression
  • T wave inversion (like ischemia)
  • PR interval prolongation (1st degreee AV block)
19
Q

Describe in an overview how the stages of MI change ECG:

A
  • Ischemia (T wave)
  • Injury (ST segment)
  • Infarction (QRS complex)
20
Q

Describe the sequence of events found in MI ECG changes:

A
  • 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

21
Q

How big must the ST segment shift be to be regarded as sig?

A

> 1mm

22
Q

How does ST depression occur?

A

Current between two regions with different potentials

23
Q

Describe the mechanism of how ischemia leads to altered ST shape:

A

Ischemia: Lowers RMP, Shortens AP, changes AP plateau

- Voltage gradient, current flow, measured / reflected by ST segment changes

24
Q

Whats diastolic and systolic current of injury?

A
  • Injury current occurs during diastole and is seen during ST
  • Injury current occurs during plateau and is seen during ST (True ST)
25
Q

What is the mechanism of MI changes to QRS?

A

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

26
Q

What doe leads opposite the infarct see?

A

Leads opposite infarct see inverse changes

  • ST depression instead of elevation
  • Tall T waves instead of inverted.

Cardiovascular MBCHB2 (31 decks)

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