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Year 2 Med > ECG > Flashcards

ECG Flashcards

1
Q

What are the axis of the ECG leads?

A
  • Axis refers to the overall electrical direction within the heart.
  • Electricity moving towards an electrode is POSITIVE
  • Electricity moving away from an electrode is NEGATIVE
  • If there is a change in the overall direction of the energy, the axis will be described as deviated- left, or right
  • Look at leads I and II. If both are positive, the axis is normal
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2
Q

What do the different areas of the ECG mean?

A
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3
Q

How to calculate rate in ECG?

A
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4
Q

What is a normal PR interval?

A

Upright P wave=sinus

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5
Q

What is a normal QRS complex?

A
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6
Q

What is a normal ST segment?

A

Depression=angina

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7
Q

What is a normal T wave?

A
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8
Q

What is a normal QT interval?

A

Long QT=danger for arrhythmia

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9
Q

How do you read an ECG?

A
  1. Is the rhythm regular or irregular?
  2. Is the heart rate fast or slow?
  3. Is the axis in Lead I & II positive?
  4. Ratio; Is there one ‘p’ wave to each QRS?
  5. Is there any ST elevation or depression?
  6. Check intervals (PR, QRS, QT)
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10
Q

Appearance of rhythms above vs below AV node

A
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11
Q

What does a normal sinus rhythm look like?

A

Normal rate = 60-100

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12
Q

What does atrial fibrillation look like?

A
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13
Q

What does atrial flutter look like?

A
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14
Q

What does heart block look like?

A
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15
Q

What does tachycardia look like?

A
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16
Q

What does ischaemia look like?

A
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17
Q

What does a MI look like?

A
18
Q

STEMI vs NSTEMI

A
19
Q

What are cardiac arrhythmias?

A
  • An abnormality of the cardiac rhythm is called a cardiac arrhythmia.
  • Arrhythmias may cause sudden death, syncope, heart failure, chest pain, dizziness, palpitations or no symptoms at all.
  • There are two main types of arrhythmia:
    • Bradycardia: the heart rate is slow (<60b.p.m. during the day or
    <50b.p.m. at night).
    • Tachycardia: the heart rate is fast (>100b.p.m.).
  • Tachycardias are more symptomatic when the arrhythmia is
    fast and sustained.
  • Tachycardias are subdivided into:
    • supraventricular tachycardias (SVT), which arise from the atrium
    or the AV junction
    • ventricular tachycardias, which arise from the ventricles.
  • Some arrhythmias occur in patients with apparently normal
    hearts or originate from diseased tissue (scar) because of
    underlying structural heart disease.
  • When myocardial function is poor, arrhythmias are more
    symptomatic and are potentially life-threatening
20
Q

What are sinus arrhythmias?

A
  • Fluctuations of autonomic tone result in phasic changes of
    the sinus discharge rate.
  • During inspiration, parasympathetic tone falls, and the heart
    rate quickens; on expiration, the heart rate falls.
  • This variation is normal, particularly in children and young adults.
  • Typically, sinus arrhythmia results in predictable irregularities of the pulse
21
Q

What are the mechanisms for arrhythmia production?

A
22
Q

What is accelerated automacity?

A
23
Q

What is triggered activity?

A
  • Is always preceded by AP
  • Caused by afterdepolarizations
  • 2 types:
    • early afterdepolarizations (EADs)
    • delayed afterdepolarizations (DADs)
  • EADs may appear either at the end of the action potential plateau
    (phase 2) or approximately midway through repolarization (phase 3)→ prolonged QT, Torsade’s de pointes
  • DADs occur near the very end of repolarization or just after full repolarization (phase 4)→ Ectopic beat, VT
24
Q

What is the aetiology of triggered activities and what are the consequences?

A

Causes of EADs:

  1. Slow HR
  2. Prolonged action potentials.
  3. Certain antiarrhythmic drugs like quinidine which prolongs the
    action potential.

Causes of DADs:

  1. Increased serum Calcium Activate a 3Na+/Ca2+ exchanger
  2. Increased Adrenaline
  3. Drug Toxicity like Digoxin
  4. Myocardial Infarction
25
Q

What is re-entry?

A
  • Requirements for re-entry
  • Two possible routes for electrical impulse to flow down
    • Fast-pathway →Long RP
    • Slow-pathway →Short RP
  • Impulse flows down one pathway, back up the other, and gets caught in a loop.
  • Slower pathway/route can be caused by:
    1. Central area of block e.g. scar tissue, refractory cells
    2. Area/path of variable blocking e.g. dead myocyte, myocytes with
    different RP/conduction speed
26
Q

What is sinus bradycardia and its causes?

A

Sinus bradycardia

  • Sinus bradycardia is due either to extrinsic factors that influence a relatively normal sinus node, or to intrinsic sinus node disease.
  • The mechanism can be acute and reversible, or chronic and degenerative.
  • Common extrinsic causes:
    • hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure
    • drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs
    • neurally mediated syndromes (carotid sinus syndrome, vasovagal attacks)
  • Common intrinsic causes:
    • acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction)
    • chronic degenerative changes, such as fibrosis of the atrium and sinus node (sick sinus syndrome)
27
Q

What is heart block?

A
  • Block in either the AV node or the His bundle results in AV block
  • Block lower in the conduction system produces bundle
    branch block.
  • 3 forms:
    1. First-degree
    2. Second-degree
    3. Third-degree
28
Q

What is first degree heart block?

A
29
Q

What is second degree heart block?

A

Due to a block at an infranodal level, such as the His bundle. Pacing usually indicated.

30
Q

Type 1 vs 2 second degree heart block

A
31
Q

What is third degree heart block?

A
32
Q

What is the aetiology of complete block?

A
  • Congenital: transposition of great vessels
  • Idiopathic fibrosis: Lev’s disease (older people), Lenegre’s disease (younger people)
  • IHD: acute MI, ischaemic cardiomyopathy
  • Non-IHD: Calcific aortic stenosis, Idiopathic dilated cardiomyopathy, Infiltrations (e.g. amyloidosis, sarcoidosis, neoplasia)
  • Cardiac surgery: Following aortic valve replacement, CABG, VSD repair
  • Iatrogenic: Radiofrequency AV node ablation and pacemaker implantation
  • Drug-induced: Digoxin, beta-blockers, amiodarone, non-dihydropyridine calcium- channel blockers
  • Infection: Endocarditis, lyme disease, chagas’ disease
  • Autoimmune: SLE, RA
  • Neuromuscular disease: Duchenne muscular dystrophy
33
Q

What is the pathophysiology of complete block?

A
  • Complete heart block occurs when there is complete dissociation
    between atrial and ventricular activity
  • P waves and QRS complexes occur independently of one another
  • Ventricular contractions are maintained by a spontaneous escape
    rhythm originating below the site of the block either from:
    • His bundle: narrow complex QRS (<0.12 s), rate 50–60 bpm, if due to transient ischaemia, IV atropine (no need for pacing), if chronic then pacing
    • His-Purkinje system: broad QRS complex (>0.12 s), rate <40 bpm, associated with dizziness and blackouts (Stokes–Adams attacks), Lev’s disease in elderly and Lenegre’s disease in younger pt., permanent pacemaker indicated
34
Q

What is bundle branch block?

A
35
Q

What are the narrow complex tachycardias?

A
36
Q

What is atrioventricular nodal re-entrant tachycardia?

A

Anterograde re-entry; from atrium to ventricle. Red is delta wave

37
Q

AVRT vs AVNRT

A
38
Q

What is atrial flutter

A
39
Q

What is atrial fibrillation?

A
40
Q

Atrial fibrillation vs flutter

A
  • Definition:
    • Flutter: Regular, rapid atrial contractions at a rate of 250-350
    beats per minute.
    • Fibrillation: Chaotic, irregular atrial contractions at rates
    exceeding 300 beats per minute
  • ECG:
    • Flutter: Sawtooth (F waves), typically in a 2:1, 3:1, or 4:1 conduction ratio.
    • Fibrillation: ƒ waves, no P waves, irregularly irregular rhythm.
  • Symptoms:
    • Flutter: palpitations, chest discomfort, and fatigue.
    • Fibrillation: palpitations, dyspnoea, dizziness, and fatigue.
  • Complications:
    • Flutter: Less commonly associated with embolic events compared to atrial fibrillation.
    • Fibrillation: Higher risk of embolic events and stroke due to blood stasis in the atria.
  • Management:
    • Flutter: rate control medications or rhythm control such as ablation.
    • Fibrillation: rate control, anticoagulation, and rhythm control based on patient characteristics.
  • Prognosis:
    • Flutter: Generally considered less severe compared to atrial
    fibrillation in terms of thromboembolic risk.
    • Fibrillation: Higher risk of complications like stroke and heart
    failure compared to atrial flutter.
41
Q

What part of an ECG refers to which part of conduction?

A

Year 2 Med (60 decks)

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