Abnormal EKG's

Dr. Hang TranEmergency Medicine Resident PGY-3

St. Vincent Mercy Medical CenterToledo, OHApril 2011

Interpretation?

Normal EKG

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Sinus Tachycardia

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Sinus Bradycardia with T wave Inversions

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1st Degree AVB

1st Degree AVB

• PR prolongation

• Disease of electrical conduction system PR interval > 0.20 seconds

• Impulse from atria to ventricles through AV node is delayed

• Causes

– Most common cause is enhanced vagal tone (ex athletes)

– Myocarditis

– Acute myocardial infarction (esp acute inferior MI)

– Electrolyte disturbances

– Medication

Interpretation?

2nd Degree AVB Type 1

2nd Degree AVB Type 1 Mobitz 1 or Wenckebach

- When one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction.

- Mobitz I heart block is characterized by progressive prolongation of the PR interval on the ECG on consecutive beats followed by a blocked P wave (i.e., a 'dropped' QRS complex)

- It is almost always a disease of the AV node.

- This is almost always a benign condition for which no specific treatment is needed.

Interpretation?

2nd Degree AVB Type 2Mobitz II

2nd Degree AVB Type 2Mobitz II

- Almost always a disease of the distal conduction system (His-Purkinje System.

- intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening.

- The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge. In this case, the person may experience, cardiac arrest, or sudden cardiac death.

- The definitive treatment for this form of AV Block is an implanted pacemaker.

Interpretation?

3rd Degree AVBComplete Heart Block

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Nonsustained VTach

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Monomorphic VTach

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Ventricular Fibrillation

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Atrial Flutter with Variable Conduction

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Atrial Flutter 3:1

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Afib with Rapid Ventricular Response (RVR)

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Anterior STEMI

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Inferior STEMI

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Inferior Posterior STEMI

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Posterior MI

Posterior MI - Posterior Leads

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Left Ventricular Aneurysm

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LBBB

LBBB

• Criteria for LBBB

– QRS >0.12 sec

– Broad monomorphic R waves in I and V6 with no Q waves

– Broad monomorphic S waves in V1, may have a small r wave

• Causes of LBBB

– Aortic stenosis

– Dilated cardiomyopathy

– Acute myocardial infarction

– Primary disease of cardiac conduction system

– Long standing hypertension

Interpretation?

RBBB

RBBB

- The QRS duration must be > 100 ms (incomplete block) or > 120 ms (complete block).

- There should be a terminal R wave in lead V1 (e.g. RSR')

- There should be a slurred S wave in leads I and V6.

- Causes

- Congenital lesions

- Primary pulmonary disease

- Pulmonary emboli

- Ischemic heart disease

- Myocarditis

Interpretation?

Brugada Syndrome

Brugada Syndrome

- Brugada is a genetic disease that is characterised by abnormal ECG findings and an increased risk of sudden cardiac death. 20% of the cases are found to have a mutation in the gene for sodium ion channel in the myocytes.

- The episodes of syncope and sudden death are caused by fast polymorphic ventricular tachycardias or ventricular fibrillation. These arrhythmias appear with no warning.

- While there is no exact treatment modality that reliably and totally prevents ventricular fibrillation from occurring, treatment lies in termination of this lethal arrhythmia before it causes death with implantation of automatic implanted cardioverter defibrillator (AICD).

Brugada Morphology

Interpretation?

Wolff Parkinson White

Wolff Parkinson White

- Syndrome of pre-excitation of ventricles of the heart due to an accessory pathway known as the bundle of Kent. This accessory pathway is an abnormal electrical communication from the atria to the ventricles.

- Sudden deathdue to WPW syndrome is rare (incidence of < 0.6%), and is due to the effect of the accessory pathway on tachyarrhythmias in these individuals.

- Delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node.

WPW Accessory Pathway

Wolff Parkinson White

- Treatment with amiodarone or procainamide in WPW patients with afib with RVR

- Cardioversion in unstable patients, those with altered mental status, lethargy or hypotension.

- Avoid agents that block the AV node, this includes adenosine, calcium channel blockers, and beta blockers.

- The definitive treatment of WPW syndrome is a destruction of the abnormal electrical pathway by radiofrequency catheter ablation.

Interpretation?

Lown Ganong Levine Syndrome

Lown Ganong Levine Syndrome

- Syndrome of pre-excitation of the ventricles due to an accessory pathway that connects the atria directly to the bundle of His providing an abnormal electrical communication.

- LGL manifest as a PR interval less than or equal to 0.12 second with normal QRS complex duration.

- It is distinguished from WPW

- The QRS complexes in LGL syndrome are normal because ventricular contraction is initiated in the normal manner. The broad complexes seen in the asymptomatic individual with WPW are not a feature of LGL.

- The delta waves seen in WPW syndrome are not seen in LGL syndrome as the accessory pathway does not connect to the ventricles and so ventricular contraction does not start early.

Interpretation?

Pericarditis

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Pulmonary Embolism

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Wellen's Syndrome

Wellen's Syndrome

- Progressive symmetrical deep T wave inversion in leads V2 and V3.

- Associated with stenosis of the left anterior descending artery with complete or near-complete occlusion in 59%. In the original Wellens' study group 75% of those with the typical syndrome manifestations had an anterior myocardial infarction. Sensitivity and specificity for significant (more or equal to 70%) stenosis of the LAD artery was found to be 69% and 89% respectively with positive predictive value 86%

Wellen's Biphasic T Waves

Interpretation?

Intracerebral Bleed

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