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NUR5925 > - ADVANCED ECG INTERPRETATION - > Flashcards

- ADVANCED ECG INTERPRETATION - Flashcards

1
Q

Discuss the phases of the action potential of myocardial cells

A

Phase 0 - Rapid depolarisation (influx of Na+) Phase 1 - Partial repolarisation (deactivation of Na+ influx and eflux of K+) Phase 2 - Plateau (slow influx of Ca2+, equals the efflux of K+) Phase 3 - Repolarisation (deactivation of Ca2+ influx, K+ eflux) Phase 4 - Pacemaker potential (slow influx of Na+ which slows the eflux of K+, “autorhythmicity”) Refractory period - Phases 1-3

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2
Q

Discuss the sodium cycle in the myocardial cells

A

-.The sodium pump is responsible for the initiation of the action potential - It is voltage dependant and thus sodium moves rapidly - These channels are open during phase 0, allowing for the rapid influx of sodium ions - This influx causes an increase in the membrane potential4 - As the membrane potential increases the sodium channels close again - During this inactivation state sodium cannot pass through the membrane ( this is relevant for the absolute refractory period phases 1-3)

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3
Q

Discuss the calcium cycle in myocardium cells

A

.- There is an influx of Calcium in phase 2 which is steady and equals the potassium out, resulting in a plateau - the influx of calcium is largely responsible for contraction of the muscle - there are 2 types of calcium channels T and L type channels - T channels act faster and contribute to depolarisation, phase 0, and L channels are active in phase 2, plateau phase, and allow for a slow influx of calcium

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4
Q

Discuss depolarisation, repolarisation and resting membrane potential of myocardial cells

A

.Depolarisation - phase 0 (action potential triggered by neighbouring cells through gap junctions, raises transmembrane potential, Fast Na+ channels open and rapid influx of sodium, increasing the voltage of the cell Repolarisation - Early repolarisation in phase 1 as som potassium leaks out of the cell, full repolarisation in phase 3 as the calcium channels are closed and potassium continues to leak out bringing the voltage back down to -90mv

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5
Q

Discuss the absolute, effective and relative refractory periods of myocardial cells as well as supra

A

.Absolute refractory period (ARP): the cell is completely unexcitable to a new stimulus. Phase 2. Effective refractory period (ERP): ARP + short segment of phase 3 during which a stimulus may cause the cell to depolarize minimally but will not result in a propagated action potential (i.e. neighbouring cells will not depolarize). Relative refractory period (RRP): a greater than normal stimulus will depolarize the cell and cause an action potential. Phase 3. Supranormal period: a hyperexcitable period during which a weaker than normal stimulus will depolarize the cells and cause an action potential. Cells in this phase are particularly susceptible to arrhythmias when exposed to an inappropriately timed stimulus, which is why one must synchronize the electrical stimulus during cardioversion to prevent inducing ventricular fibrillation.

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6
Q

Define axis deviation

A

The electric axis of the heart is the net direction in which the wave of depolarisation travels.

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7
Q

Discuss how to identify left and right axis deviation

A

RAD: Lead I - negative avF/III - positive LAD: Lead I - positive avF/III - negative

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8
Q

Discuss the causes of left/right axis deviation

A

Right axis deviation (RAD): Right ventricular hypertrophy Acute right ventricular strain, e.g. due to pulmonary embolism Lateral STEMI Chronic lung disease, e.g. COPD Hyperkalaemia Sodium-channel blockade, e.g. TCA poisoning Wolff-Parkinson-White syndrome Dextrocardia Ventricular ectopy Secundum ASD – rSR’ pattern Normal paediatric ECG Left posterior fascicular block – diagnosis of exclusion Vertically orientated heart – tall, thin patient Left Axis Deviation (LAD): Left ventricular hypertrophy Left bundle branch block Inferior MI Ventricular pacing /ectopy Wolff-Parkinson-White Syndrome Left anterior fascicular block – diagnosis of exclusion Horizontally orientated heart – short, squat patient Extreme axis deviation: Ventricular rhythms – e.g.VT, AIVR, ventricular ectopy Hyperkalaemia Severe right ventricular hypertrophy

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9
Q

Outline the criteria to identify ST elevation (and lead groupings)

A

.o ≥2 mm of ST segment elevation in 2 contiguous precordial leads in men (1.5 mm for women) o ≥1mm in other leads (2 contiguous) o An initial Q wave or abnormal R wave develops over a period of several hours to days.

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10
Q

Outline the ECG lead groupings

A

Inferior - Lead II, III, and avF Lateral - Lead I, avL, V5, V6 Anterior - V3, V4 Septal - V1, V2

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11
Q

Outline the criteria to identify 1st degree block

A
  • PR interval > 200ms (five small squares) - ‘Marked’ first degree block if PR interval > 300ms - P waves buried in preceding T waves
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12
Q

Outline the criteria to identify 2nd degree block (Mobitz I) (Wenckebach)

A
  • Progressive prolongation of the PR interval culminating in a non-conducted P wave - The PR interval is longest immediately before the dropped beat - The PR interval is shortest immediately after the dropped beat
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13
Q

Outline the criteria to identify 3rd degree block ( complete heart block)

A
  • atrial and ventricular pacing is regular but completely unrelated to one another - two seperate, regular rates - .None of the atrial impulses appear to be conducted to the ventricles. - Rhythm is maintained by a junctional escape rhythm.
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14
Q

Outline the criteria to identify supraventricular tachycardia

A
  • P waves are often hidden – being embedded in the QRS complexes. - Pseudo R’ wave may be seen in V1 or V2. - Pseudo S waves may be seen in leads II, III or aVF. - In most cases this results in a ‘typical’ SVT appearance with absent P waves and tachycardia
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15
Q

Outline the criteria to identify left bundle branch block

A
  • QRS duration of > 120 ms - Dominant S wave in V1 - Broad monophasic R wave in lateral leads (I, aVL, V5-V6) - Absence of Q waves in lateral leads (I, - V5-V6; small Q waves are still allowed in aVL) - Prolonged R wave peak time > 60ms in left precordial leads (V5-6) - Appropriate discordance: the ST segments and T waves always go in the opposite direction to the main vector of the QRS complex - Poor R wave progression in the chest leads - Left axis deviation
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16
Q

Outline the criteria to identify right bundle branch block

A
  • Broad QRS > 120 ms - RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) - Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
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17
Q

Outline the criteria to identify left anterior fascicular block (LAFB)

A
  • Left axis deviation (usually between -45 and -90 degrees) - Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL - Small R waves with deep S waves (= ‘rS complexes’) in leads II, III, aVF - QRS duration normal or slightly prolonged (80-110 ms) - Prolonged R wave peak time in aVL > 45 ms - Increased QRS voltage in the limb leads
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18
Q

Outline the criteria to identify left posterior fascicular block (LPFB)

A
  • Right axis deviation (> +90 degrees) - Small R waves with deep S waves (= ‘rS complexes’) in leads I and aVL - Small Q waves with tall R waves (= ‘qR complexes’) in leads II, III and aVF - QRS duration normal or slightly prolonged (80-110ms) - Prolonged R wave peak time in aVF - Increased QRS voltage in the limb leads - No evidence of right ventricular hypertrophy - No evidence of any other cause for right axis deviation
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19
Q

Outline the criteria to identify a bifascicular block

A
  • Bifascicular block is the combination of RBBB with either LAFB or LPFB. - Conduction to the ventricles is via the single remaining fascicle. - The ECG will show typical features of RBBB plus either left or right axis deviation. - RBBB + LAFB is the most common of the two patterns.
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20
Q

Outline the criteria to identify a trifascicular block

A

.Trifascicular block (TFB) refers to the presence of conducting disease in all three fascicles: - Right bundle branch (RBB) - Left anterior fascicle (LAF) - Left posterior fascicle (LPF) The most common is a combination of bifascicular block with 1st degree AV block. Incomplete trifascicular block: - Bifascicular block + 1st degree AV block (most common) - Bifascicular block + 2nd degree AV block - RBBB + alternating LAFB / LPFB Complete trifascicular block: - Bifascicular block + 3rd degree AV block

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21
Q

Outline the criteria to identify wolf parkinson white

A
  • Wolff-Parkinson-White (WPW) Syndrome is a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia - PR interval <120ms - Delta wave – slurring slow rise of initial portion of the QRS - QRS prolongation >110ms - ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex
22
Q

Outline the criteria to identify an accelerated idioventricular rhythm

A
  • Regular rhythm. - Rate 50-110 bpm. - Three or more ventricular complexes. - QRS complexes >120ms. - Fusion and capture beats.
23
Q

Outline the criteria to identify accelerated junctional rhythm

A
  • Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction). 0
  • Ventricular rate usually 60 – 100 bpm.
  • Retrograde P waves may be present and can appear before, during or after the QRS complex.
  • Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR + V1.
  • AV dissociation may be present with the ventricular rate usually greater than the atrial rate.
  • There may be associated ECG features of digoxin effect or digoxin toxicity.
24
Q

Outline the criteria to identify dilated cardiomyopathy

A

. - The most common ECG abnormalities are those associated with atrial and ventricular hypertrophy — typically, left sided changes are seen but there may be signs of biatrial or biventricular hypertrophy. - Interventricular conduction delays (eg. LBBB) occur due to cardiac dilatation.

25
Q

Outline the criteria to identify hyperkalaemia

A

.Peaked t wave - t wave can be bigger than QRS in lead II

26
Q

Describe the mechanism of arrythmia formation

A

.Arrythmias are usually due to: - Impaired automaticity: problems with impulse formation - Abnormal impulse conduction – conduction block or reentry - Triggered activity

27
Q

Compare the ECG characteristics of a left and a right bundle branch block

A
  1. LBBB: monophasic, negative QRS in V1 RBBB: biphasic QRS ‘RSR’ in lead V1 2. In an RBBB, the S-wave is slurred while in an LBBB there are broad R-waves with the absence of Q-waves. 3. Both should have more than 0.12 seconds of QRS waves.
28
Q

Outline the significance of a left bundle branch block in an acute MI

A
  • In patients with left bundle branch block (LBBB) or ventricular paced rhythm, the baseline ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”), which can mask or mimic acute myocardial infarction. - A new LBBB is always pathological and can be a sign of myocardial infarction. - Use of the Sgarbossa criteria is used for diagnostic accuracy: - ≥ 1 lead with ≥1 mm of concordant ST elevation - ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression - ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave.
29
Q

Explain the ECG criteria pertaining to hemiblocks

A

left anterior hemiblock: - QRS axis more left than -30 degrees - initial R wave in the inferior leads (II, III and aVF) - absence of any other cause of left axis deviation

30
Q

Outline the significance and nursing management of 1st degree heart block

A

1st degree block: - Does not cause haemodynamic disturbance - No specific treatment is required

31
Q

Discuss the characteristics, description, and significance of ST elevation

A

CRITERIA FOR A STEMI: .o ≥2 mm of ST segment elevation in 2 contiguous precordial leads in men (1.5 mm for women) o ≥1mm in other leads (2 contiguous) o An initial Q wave or abnormal R wave develops over a period of several hours to days.

32
Q

Discuss the characteristics, description, and significance of pathological Q waves from a non-pathological Q waves

A

Q waves are considered pathological if: - > 40 ms (1 mm) wide - > 2 mm deep - > 25% of depth of QRS complex - Seen in leads V1-3 Pathological Q waves usually indicate current or prior myocardial infarction.

33
Q

Discuss the characteristics, description, and significance of abnormal QRS complexes

A
  1. Width of the complexes: - think: LBBB, RBBB, hyperkalaemia, tricyclic poisoning, WPW, ventricular pacing, hypothermia 2. Narrow versus broad. Voltage (height) of the complexes: - think: left ventricular hypertrophy, massive pericardial effusion, slim/athletic build ********note****** Sokolov-Lyon criteria (S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm).
34
Q

Discuss the characteristics, description, and significance of abnormal P waves (including ectopic P waves)

A
  • P mitrale (bifid P waves), seen with left atrial enlargement. - P pulmonale (peaked P waves), seen with right atrial enlargement. - P wave inversion, seen with ectopic atrial and junctional rhythms. - Variable P wave morphology, seen in multifocal atrial rhythms.
35
Q

Discuss the characteristics, description, and significance of abnormal T waves (including R wave progression)

A
  • Hyperacute T waves (STEMI, Prinzmetal angina) - Inverted T waves (normal in paeds, MI, BBB, PE, hypertrophy, raised ICP) - Biphasic T waves (ischaemia, hypokalaemia) - ‘Camel Hump’ T waves (prominant u waves - hypokalaemia, or hidden p waves - heart blocks) - Flattened T waves (ischaemia, hypokalaemia)
36
Q

Discuss the characteristics, description, and significance of premature atrial contraction

A

PACs - An abnormal (non-sinus) P wave is followed by a QRS complex (unifocal - abnormal p waves the same in morphology, multifocal - varying morphologies) ****bigeminy, trigeminy, quadrigeminy, couplet, triplet - not usually requiring investigation or treatment but may be the trigger for the onset of a re-entrant tachydysrhythmia

37
Q

Identify the mechanism, characteristics and nursing management of the narrow complex tachycardia, sinus tachycardia

A

. - Can be AV node independent (ST, AT, AF, AFlutter), or AV node dependent (AVNRT, AVRT, juctional tachycardia) - Treatment is different for each type of narrow complex tachycardia: - vagal manoeuvre adenosine 6-12mg IV (half dose if cardiac transplant or on dipryidamole) -> AV node independent: decreased AV node conduction but tachycardia persists -> AV node dependent: arrhythmia ceases

38
Q

Identify the mechanism, characteristics and nursing management of the narrow complex tachycardia, atrial flutter with a 2:1 block

A

Characteristics: - Narrow complex tachycardia at 150 bpm (range 130-170; with 2:1 AV block) - Turn the ECG upside down and scrutinise the inferior leads (II, III + aVF) for flutter waves Management: - Vagal Manoeuvres +/- Adenosine (Atrial flutter will not usually cardiovert with these techniques (unlike AVNRT), although typically there will be a transient period of increased AV block during which flutter waves may be unmasked)

39
Q

Identify the mechanism, characteristics and nursing management of the narrow complex tachycardia, AV nodal re-entry tachycardia

A
  • .vagal manoeuvres - adenosine - verapamil - sotalol - amiodarone - flecanide - overdrive pacing - cardioversion
40
Q

Identify the mechanism, characteristics and nursing management of the narrow complex tachycardia, accessory pathway AV re-entry tachycardia

A

. - vagal manoeuvres - adenosine - sotalol - amiodarone - flecanide - overdrive pacing - cardioversion -> same as AVNRT Tx EXCEPT avoidance of verapamil as leads to rapid conduction down accessory pathway (WPW).

41
Q

Identify the predisposing factors, mechanism, characteristics and management of monomorphic VT

A
  • Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”) - The presence of pre-existing poor ventricular function is strongly associated with cardiovascular compromise. - Decreased cardiac output may result in decreased myocardial perfusion with degeneration to VF - Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in all cases of VT Classified based on morphology, is it SUSTAINED? (>30sec), is it STABLE? (haemodynamically)
42
Q

Identify the predisposing factors, mechanism, characteristics and management of polymorphic VT and Torsade de point

A
  • TdP is often short lived and self terminating, however can be associated with hemodynamic instability and collapse. TdP may also degenerate into ventricular fibrillation (VF) - Can occur secondary to drug effects, electrolyte abnormalities, and medical conditions - Management strategies revolve around treating the cause (magnesium, isoprenaline, overdrive pacing, etc)
43
Q

Identify the ECG characteristics indicative of electrolyte imbalances

A

Hypokalaemia - Long QU interval, prominant U waves Hyperkalaemia - peaked T-waves Hypocalcaemia - prolonged QT Hypercalcaemia - shortening of ST segment

44
Q

Discuss the significance of a prolonged QT interval

A

The QT interval should be measured in either lead II or V5-6 and be greater than…….. Causes: - Hypokalaemia - Hypomagnesaemia - Hypocalcaemia - Hypothermia - Myocardial ischemia - Post-cardiac arrest - Raised intracranial pressure - Congenital long QT syndrome - DRUGS ***Increased risk of ventricular arrythmias esp. torsades de pointes

45
Q

Discuss the potassium cycle in myocardial cells

A
  • Two types of potassium channels (inward rectifiers and voltage-gated potassium channels) - inward rectifiers allow potassium inward during phase 4 to be in normal state - voltage-gated channels allow for the efflux of potassium through phases 1-3
46
Q

Outline the criteria for ST depression

A
  • ST depression can be either upsloping, downsloping, or horizontal (see diagram below). - Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria). - ST depression ≥ 1 mm is more specific and conveys a worse prognosis. - ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (35% mortality at 30 days). - Upsloping ST depression is non-specific for myocardial ischaemia.
47
Q

Outline the criteria to identify 2nd degree block (Mobitz II)

A
  • Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I). - The PR interval in the conducted beats remains constant. - The P waves ‘march through’ at a constant rate. - The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).
48
Q

Outline the significance and nursing management of 2nd degree block (Mobitz I/wenckebach):

A
  • usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block. - Asymptomatic patients do not require treatment. Symptomatic patients usually respond to atropine. Permanent pacing is rarely required.
49
Q

Outline the significance and nursing management of 2nd degree block (Mobitz II)

A
  • Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block. - Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death. - The risk of asystole is around 35% per year. - Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.
50
Q

Outline the significance and nursing management of 3rd degree heart block (CHB)

A
  • Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death. - They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker.
51
Q

Discuss the characteristics, description, and significance of premature ventricular contraction

A

PVC Criteria: - Broad QRS complex (≥ 120 ms) with abnormal morphology. - Premature — i.e. occurs earlier than would be expected for the next sinus impulse. - Discordant ST segment and T wave changes. - Usually followed by a full compensatory pause. - Retrograde capture of the atria may or may not occur - can be unifocal or multifocal and can originate from right or left ventricle (will be same pattern as LBBB or RBBB) - not requiring investigation or treatment, but may trigger the onset of a re-entrant tachydysrhythmia — e.g. VT, AVNRT/AVRT

NUR5925 (27 decks)

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