EKG og arytmier

Question 1

Hva ser du her?

Answer 1

Ventricular rhythm at 60 bpm.

Multiple sinus capture beats.

Competing sinus and idioventricular pacemakers are present. There is underlying sinus arrhythmia, with sinus capture occurring when the sinus rate exceeds the idioventricular rate.

This patient was a healthy 36-year old marathon runner with presumably very high resting vagal tone causing sinus bradycardia and sinus arrhythmia.

Dette er : Accelerated Idioventricular Rhythm (AIVR)

AIVR results when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node.

Often associated with increased vagal tone and decreased sympathetic tone.

Proposed mechanism is enhanced automaticity of ventricular pacemaker, although triggered activity may play a role especially in ischaemia and digoxin toxicity.

AIVR is classically seen in the reperfusion phase of an acute STEMI, e.g. post thrombolysis.

Usually a well-tolerated, benign, self-limiting arrhythmia.

• Regular rhythm.
• Rate 50-110 bpm.
• Three or more ventricular complexes.
• QRS complexes >120ms.

Question 2

dx?

Answer 2

Accelerated Idioventricular Rhythm (AIVR)

Ventricular rhythm at 75 bpm.

AV dissociation — a dissociated P wave is seen in the rhythm strip, another in lead aVL. Elsewhere, dissociated P waves cause intermittent deformation of the QRS complexes.

The taller left rabbit ear sign is present — there is a notched R wave in V1 with a taller initial R wave; this is highly specific for a ventricular origin of the QRS complexes.

Question 3

Hva er Accelerated Junctional Rhythm (AJR) ?

Answer 3

Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the sinus node.

This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node.

Ses ved:

• Digoxin toxicity (= the classic cause of AJR)
• Beta-agonists, e.g. isoprenaline, adrenaline
• Myocardial ischaemia
• Myocarditis
• Cardiac surgery

Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction).

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.

Question 4

Hva skjer her? Og hvordan kjenner man det igjen på EKGet?

Answer 4

Hyperacute Anteroseptal STEMI

• ST elevation is maximal in the anteroseptal leads (V1-4).
• Q waves are present in the septal leads (V1-2).
• There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.
• There are hyperacute (peaked ) T waves in V2-4.
• These features indicate a hyperacute anteroseptal STEMI

Hvordan kjenne igjen et akutt fremreveggs STEMI?

• ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
• Reciprocal ST depression in the inferior leads (mainly III and aVF).

Question 5

Hva er Wellens syndrome? ( vises her på EKG-et) og hva tyder det på? ( kan også ses ved flere andre tilstander)

Answer 5

Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD).

Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.

Due to the critical LAD stenosis, these patients usually require invasive therapy, do poorly with medical management and may suffer MI or cardiac arrest if inappropriately stress tested.

Kriterier:

Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)

Isoelectric or minimally-elevated ST segment (< 1mm)

No precordial Q waves

Preserved precordial R wave progression

Recent history of angina

ECG pattern present in pain-free state

Normal or slightly elevated serum cardiac markers

Question 6

Hva skjer her?

Answer 6

Hyperacute Anterior STEMI

There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of R wave height.

The rhythm is sinus with 1st degree AV block.

There are premature atrial complexes (beat 4 on the rhythm strip) and multifocal ventricular ectopy (PVCs of two different types), indicating an “irritable” myocardium at risk of ventricular fibrillation.

Question 7

God stemning eller dårlig stemning?

Answer 7

Dårlig.

Massive ST elevation with “tombstone” morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL).

This pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of cardiogenic shock and death.

Question 8

Hvilke funn ved EKG kan tyde på venstre ventrikkel hypertrofi?

Answer 8

• Increased R wave peak time > 50 ms in leads V5 or V6
• ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
• Cornell = R i Avl + Sv3 * qrs-lengde = > 2440 med mer x msek.