CVS 13 - Interpreting ECG's (Part 2) Flashcards

1
Q

What does the QT interval denote?
How long should the corrected QT interval (QTc) be?
What does a prolonged QTc suggest?

A
  • QT interval is the time for depolarisation + repolarisation of the ventricles. Varies with HR so is corrected for HR (QTc)
  • Upper limit of QTc is 0.44-0.45 seconds (11 small boxes)
  • Prolonged ventricular repolarisation - associated risk for dangerous arrhythmia.
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2
Q

What are the ECG characteristics of a normal sinus rhythm? (5 characteristics)

A
  • Regular HR of 60-100bpm
  • Each QRS complex is preceded by a normal P-wave
  • Normal P waves, should be upright in leads l, ll + inverted in aVR
  • PR interval should remain constant
  • QRS complexes are less than 100ms wide
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3
Q

What are AV conduction blocks? (heart block)
What are the 4 types of heart block?
What are the causes of heart block?

A
  • Delay of conduction of impulses from atria to ventricles via AV node + bundle of His.
  • 1st degree, 2nd degree (Mobitz type 1 + 2) + 3rd degree
  • Degeneration of conducting system w/age, acute myocardial ischaemia, medications etc.
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4
Q

What are the ECG characteristics of all 4 types of heart block?

A

Type 1 = Normal P-waves followed by a QRS complex, but PR-interval is >0.2 seconds.

Mobitz type 1 = Successful lengthening of PR-interval until QRS complex is dropped

Mobitz type 2 = PR-intervals don’t lengthen, sudden QRS complex dropping. High risk of progression to complete heart block.

Type 3 = Atria + ventricles depolarising independently, complete failure of AV conduction. Rhythm down to 20-40bpm (ventricular pacemaker takes over) very wide QRS complex.

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5
Q

What is bundle branch block (BBB) and what are the ECG characteristics?

A
  • Delayed conduction within bundle branches (right or left)
  • P waves and PR-interval normal
  • Widened QRS complex (over 0.12 seconds) - as ventricular depolarisation now takes longer.
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6
Q

What are the 2 broad categories of arrhythmias?

What kind of QRS complexes are seen on the ECG with these 2 categories?

A

1) Supraventricular (arising from above the ventricles) - normal or narrow QRS complexes (as they tend to be tachycardias)
2) Ventricular (arising from the ventricles) - wide + bizarre QRS complexes (as normal conduction pathways not being used).

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7
Q

What are the ECG characteristics associated with atrial fibrillation (Afib)?

A
  • Arising from multiple atrial foci + rapid chaotic impulses.
  • No P-waves (just wavy baseline) + irregular R-R intervals
  • Not all impulses conducted at AV node, those that are DP ventricles normally do QRS complexes are normal.
  • Can have a slow, fast or normal HR, with either fine or course fibrillation (don’t mistake for P-waves, they are absent)
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8
Q

What are the haemodynamic effects/biggest complication with Afib?

A
  • Atrial contraction lost, atria just quiver. HR and pulse “irregularly irregular”.
  • Loss of atrial contraction increases blood stasis, can get blood clots in LA therefore, Afib is a large risk factor for ischaemic stroke secondary to emboli.
  • Most common arrhythmia in general population
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9
Q

What are premature ventricular contractions (PVC’s)?
What are the ECG characteristics associated w/PVC’s?
What can 3 or more successive PVC’s lead to?

A
  • Ectopic focus in ventricular muscle, impulses don’t spread via His-Purkinje system, so DP much slower.
  • Therefore wide QRS complexes.
  • Ventricular tachycardia (VTACH) - a dangerous rhythm with high risk of progression to Vfib.
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10
Q

What is ventricular fibrillation (Vfib)?

A
  • Abnormal, chaotic, fast ventricular depolarisation
  • Impulses from multiple ectopic sites in ventricles, no coordinated contraction of ventricles, they just quiver.
  • No CO, if sustained leads to cardiac arrest.

NB: See slide 27 for great flow chart to working out which arrhythmia is present.

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11
Q

What is the difference between myocardial ischaemia + myocardial infarction?
What are the 2 classifications of myocardial infarction?

A

Ischaemia = Lack of perfusion to muscle but no muscle necrosis. Blood tests therefore negative for troponins.

Infarction = Lack of perfusion to muscle and necrosis present. Blood tests therefore positive for troponins.

1) STEMI = ST elevation MI
2) NSTEMI - non-ST elevation MI

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12
Q

What is STEMI caused by?

What are the associated ECG changes?

A
  • Complete occlusion of coronary artery (not just partial) + full thickness of myocardium undergoes necrosis.
  • ST elevation most important sign, also get hyper-acute or inversed T-waves, and pathological Q-waves.
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13
Q

What are pathological Q-waves?

A
  • A Q-wave preceding an R wave that is >0.04 seconds wide or > 2 small squares deep. Depth is more than 1/4 of the subsequent R-wave.
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14
Q

The ECG changes in NSTEMI + unstable angina (severe ischaemia) are the same. How would you differentiate between them?

A
  • Differentiate by blood tests (presence of troponins). Present in NSTEMI not in unstable angina, as there is absence of myocardial cell death.
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15
Q

What are the ECG changes seen in NSTEMI and unstable angina (severe ischaemia)?

A
  • ST depression + T-wave inversion (normally upright in all leads except aVR + V1).
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16
Q

What are the ECG changes seen in stable angina?

A
  • ECG is normal at rest (as this won’t cause an attack)

- During exercise there is ST-depression.

17
Q

What are the signs and symptoms of hypokalaemia?

What are the associated ECG changes?

A
  • K+ level <3.5 mmol/L
  • Causes myocardial hyper-excitability - palpitations, arrhythmia, cardiac arrest
  • Increased amplitude + width of P wave, prolonged PRI, ST depression, T-wave flattening + inversion.
18
Q

What are the signs and symptoms of hyperkalaemia?

What are the associated ECG changes?

A
  • K+ levels >5mmol/L
  • Resting membrane potential less negative, causes inactivation of Na+ channels, heart less excitable, leading to palpitations, arrhythmia + cardiac arrest.
  • Tall T-waves, loss of P-wave, widened QRS (with increasing K+ concentrations).