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Rate in beats/min = 60/interval between two beats in seconds A handy shortcut is: Heart rate (beats/min) = 1500/R-R interval

(mm) 1500/20 = 75 b/min

Heart block Heart block results when conduction between the atria and ventricles is altered. This often occurs at the AV node which has a low safety factor.

First degree - prolonged PR interval only. The normal PR interval is 0.12 to 0.21 seconds. A PR interval >0.21 would be classified as first degree block. Usually this block is above His bundle

Second degree - some P waves are not followed by QRS. Often has a regular sequence, i.e., 2:1 or 3:2. The first number is the number of P waves present and the second is the number of QRSs. What is this?

Mobitz I (Wenckebach) the PR progressively lengthens with one P wave for every QRS until a beat is dropped. Usually the block is above His bundle. This is common in coronary patients and is caused by increased vagal tone and usually eventually disappears with no problems

Mobitz II the PR is constant but with occasional dropped beats. This is a more serious arrhythmia because the injury is probably in fast conducting tissue below the His bundle which is not under vagal control.

This is unambiguously Mobitz II It is a dangerous arrhythmia because the heart may suddenly start beating very slowly or even stop.

Complete heart block. Since there is no conduction down the AV node pathway atria and ventricles beat regularly but at different rates.

Slow ventricular rate Usually treated with pacemaker May be temporary or intermittent. Can be induced by drugs that cause increased vagotonia

WPW: Normally conducting cardiac muscle bridges the gap between atria and ventricles. The accessory pathway activates the ventricle before normal activation via the AV node.

The PR interval is <0.12 sec Delta waves are usually present

Can get retrograde conduction causing reentry and a tachyarrhythmia. If accessory pathway has short antegrade refractory period, can allow the ventricle to beat too fast with atrial fibrillation

Fig 3

Sinus Tachycardia >100b/min 1. Normal P waves


Normal sinus rhythm

2. Normal or shortened PR interval 3. QRS and T vectors are normal 4. ST segments are normal

Sinus tachycardia

5. RR interval short <15mm 1500/100 = 15

Sinus bradycardia

Fig 3

Sinus Bradycardia <60b/min


Normal sinus rhythm

1. P waves are present and all are followed by a QRS 2. Normal and constant PR interval 3. QRS and T vectors are normal

Sinus tachycardia

4. ST segments are normal 5. RR interval long >25mm 1500/60 = 25

Sinus bradycardia

Premature ventricular contraction (PVC) 1. Arises from ectopic focus in ventricles 2. Early QRS not preceded by a P wave (see fig 4) 3. Will have an unusual QRS shape a) odd vector b) prolonged QRS duration

Premature ventricular contraction (PVC) 1. Arises from ectopic focus in ventricles 2. Early QRS not preceded by a P wave (see fig 4) 3. Will have an unusual QRS shape a) odd vector b) prolonged QRS duration 4. A compensatory pause

Multifocal PVCs. Two separate foci are originating PVCs Irritable ventricle IF all PVC are identical it is from one ectopic site (Unifocal).

Premature atrial contraction (PAC) 1. Arises from an ectopic focus in the atria. 2. Will have an identifiable P wave but the shape of the P wave may be altered 3. May have a normal QRS 4. May have a compensatory pause

The compensatory pause is lacking because the SA node was reset. The rhythm has been shifted.

The QRS may be altered if some of the ventricle is still in its refractory period.

Atrial fibrillation 1. Irregularly irregular 2. No P waves

The AV node keeps the ventricular rate low May be treated with drugs to depress AV conduction and slow the ventricular rhythm: Beta blockers, calcium channel blockers

Common: will occur in about 1/3 of the population Not a serious arrhythmia unless in WPW

Electrical reentry can cause fibrillations and tachycardias.

Ventricular tachycardia (Fig 9) 1. Regularly occurring rhythm originating from a regular ventricular ectopic focus. 2. QRS morphology is usually like a PVC

Because the cardiac output is very low it usually produces myocardial ischemia and often progresses to ventricular fibrillation

Ventricular fibrillation (VF) 1. Thought to be a reentrant excitation of the ventricles; premature impulse may arise during vulnerable period 2. Irregular baseline with no identifiable waves

3. No cardiac output. Usually the cause of "sudden death" 4. May be the result of ischemia, lightning strike, electrocution, chest trauma, or drugs 5. Requires CPR and electrical difibrillation. Patients do not spontaneously recover.

Extended phase two cause long QT syndrome.

12 blocks

Q-T interval is ratedependent and is an index of the duration of phase 2 in the ventricular AP 12 x 40 = 480 ms

Long QT syndrome Prolonged duration of phase 2 causes an early afterdepolarization. That can trigger an early action potential causing a reentrant tachycardia Patients may experience attacks of VT with torsades de pointes - a waxing and waning of the QRS morphology (as if circling around a point).

3. Long QT is induced by some drugs and can be due to genetic abnormalities in some potassium and calcium channels. At present 5 separate genetic defects have been identified which cause long QT

14 STEPS TO ASSURE A SUCCESSFUL READING AND UNDERSTANDING OF AN UNKNOWN ECG 1. Is the ventricular rhythm regular? 2. Are there P waves? 3. Is the atrial rhythm regular? 4. Is there one P wave for each QRS? 5. What are the atrial and ventricular rates? 6. What is the P-R interval? 7. Is the P-R interval constant? 8. Are there extra or premature beats? 9. What is the QRS duration? 10. Does the QRS morphology indicate presence of a conduction defect? 11. What is the mean electrical QRS axis? 12. What is the mean electrical P wave axis? 13. Is there S-T segment deviation? 14. Are there pathologic Q waves?

Fig 12 a summary of heart blocks.

Fig 13 a summary of other arrhythmias.