Normal adult 12-lead ECG The diagnosis of the normal electrocardiogram is made by excluding any recognised abnormality. It's description is therefore quite lengthy.
Atrial Fibrillation and Old inferior myocardial infarction a Q wave in lead III wider than 1 mm (1 small square) and a Q wave in lead aVF wider than 0.5 mm and a Q wave of any size in lead II
Mitral Stenosis There is atrial fibrillation . No P waves are visible. The rhythm is irregularly irregular (random). There is the suggestion of right ventricular hypertrophy. Right axis deviation and deep S waves in the lateral leads. Another important feature of right ventricular hypertrophy not shown here is a dominant R wave in lead V1. The combination of Atrial Fibrillation and Right Axis Deviation on the ECG suggests the possibility of mitral stenosis.
Atrial fibrillation with rapid ventricular response Irregularly irregular ventricular rhythm. Sometimes on first look the rhythm may appear regular but on closer inspection it is clearly irregular.
Atrial fibrillation with pre-existing left bundle branch block Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity. Irregularly irregular rhythm - suggesting AF. Features of typical left bundle branch block wide QRS >120 ms (3 small squares) no secondary R wave in lead V1 no lateral Q waves
Atrial flutter A characteristic 'sawtooth' or 'picket-fence' waveform of an intra-atrial re-entry circuit usually at about 300 bpm. This lady was taking rather too much digoxin and has a very slow ventricular response.
Atrial flutter with 2:1 AV conduction The sawtooth waveform of atrial flutter can usually be seen in the inferior leads II, III and aVF if one looks closely. Sometimes the rapid atrial rate can be seen in V1. Suspect atrial flutter with 2:1 block when you see a rate of about 150 bpm. The atrial rate is shown to be twice the ventricular rate in the figure below. See also atrial flutter with slow ventricular response .
Long QT interval The QT interval normally varies with heart rate - becoming shorter at faster rates. It is usually corrected using the cycle length (R-R interval) as shown opposite. normal QTc = 0.42 seconds Romano-Ward syndrome is an autosomal dominantly inherited form of long QT interval and there is a risk of recurrent ventricular tachycardia, particularly Torsade de Pointes . Ventricular premature beats (VPBs) 2 ventricular premature beats are also shown in this ECG They are broad occur earlier than normal and are followed by a full compensatory pause (the distance between the normal beats before and after the VPB is equal to twice the normal cycle length).
Ventricular bigeminy a ventricular premature beat follows each normal beat There are also features of an acute inferior myocardial infarction .
Ventricular tachycardia A wide QRS tachycardia is VT until proven otherwise (1). Features suggesting VT include:- evidence of AV dissociation independent P waves (shown by arrows here) capture or fusion beats beat to beat variability of the QRS morphology very wide complexes (> 140 ms) the same morphology in tachycardia as in ventricular ectopics history of ischaemic heart disease absence of any rS, RS or Rs complexes in the chest leads (2) concordance (chest leads all positive or negative)
Ventricular tachycardia A wide QRS tachycardia is VT until proven otherwise (1). Features suggesting VT include:- evidence of AV dissociation independent P waves capture or fusion beats beat to beat variability of the QRS morphology (shown here) very wide complexes (> 140 ms) the same morphology in tachycardia as in ventricular ectopics history of ischaemic heart disease absence of any rS, RS or Rs complexes in the chest leads (2) concordance (chest leads all positive or negative)
Polymorphous ventricular tachycardia (Torsade de pointes). This is a form of VT where there is usually no difficulty in recognizing its ventricular origin. wide QRS complexes with multiple morphologies changing R - R intervals the axis seems to twist about the isoelectric line it is important to recognize this pattern as there are a number of reversible causes heart block hypokalaemia or hypomagnesaemia drugs (e.g. tricyclic antidepressant overdose) congenital long QT syndromes other causes of long QT (e.g. IHD)
Wolf-Parkinson-White syndrome short PR interval, less than 3 small squares (120 ms) slurred upstroke to the QRS indicating pre-excitation (delta wave) broad QRS secondary ST and T wave changes Localising the accessory pathway An accessory pathway, bundle of Kent, exists between atria and ventricles and causes early depolarisation of the ventricle. The location of the pathway may be deduced as follows:- LOCATION V1 V2 QRS axis left posteroseptal (type A) +ve +ve left right lateral (type B) -ve -ve left left lateral (type C) +ve +ve inferior (90 degrees) right posteroseptal -ve -ve left anteroseptal -ve -ve normal
Wolf-Parkinson-White syndrome with atrial fibrillation irregularly irregular, wide complex tachycardia impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway producing a broad fusion complex or just the AV node producing a narrow complex (without a delta wave) or just the accessory pathway producing a very broad 'pure' delta wave people who develop this rhythm and have very short R - R intervals are at higher risk of VF
2 to 1 AV block every other P wave is conducted to the ventricles 2 to 1 AV block starts after the 5th QRS in this 3 channel recording. The first non-conducted P wave is indicated with an arrow. the PR interval of conducted P waves is constant in this lady there is a long PR interval (and left bundle branch block ) 2 to 1 AV block cannot be classified into Mobitz type I or II as we do not know if the 2nd P wave would be conducted with the same or longer PR interval.
Atrial fibrillation and complete heart block Fibrillary waves of atrial fibrillation and no P waves. Regular ventricular rhythm The wider the QRS of the ventricular escape rhythm the less reliable the escape mechanism. AF with complete heart block can be easily missed and is an indication for a permanent pacemaker.
0 ecg arrhythmia for medical students samir rafla
Arrhythmia for Medical StudentsSamir Rafla, FACC, FESC Prof. of Cardiology Alexandria University
Sinus BradycardiaCardiac impulses arise in the sinus node at a rate lessthan 60/min.Etiology:A- Physiologic: Athletes, sleep, and carotid sinuscompression.B- Pharmacologic: Digitalis, propranolol, verapamiland diltiazem.C- Pathologic: Convalescence from infections,hypothyroidism, obstructive jaundice, rapid rise ofthe intracranial tension, hypothermia and myocardialinfarction (particularly inferior wall infarction)
SUPRAVENTRICULAR TACHYARRHYTHMIASSVTs may be separated into three groups based onduration: brief paroxysms, persistent, and chronic(permanent).Arrhythmias that are paroxysmal in onset and offset(e.g. paroxysmal SVT due to AV nodal reentry orWPW syndrome, paroxysmal atrial fibrillation,paroxysmal atrial flutter) tend to be recurrent and ofshort duration
Supraventricular tachyarrhythmias include: atrial tachycardia, atrial flutter, atrial fibrillation and AV tachycardias.
Management of PSVT Due to AV Nodal ReentryThe acute attack: Vagal maneuvers serve as the firstline of therapy. Simple procedures to terminateparoxysmal SVT- Carotid sinus massage: If effective the rhythm isabruptly stopped; occasionally only moderateslowing occurs- Cold water splash on face.- Performance of Valsalvas maneuver (ofteneffective).
Management of PSVT Due to AV NodalReentryIntravenous adenosine, Ca channel blockers(verapamil), digoxin or B-blockers are the choicesfor managing the acute episodes.Adenosine, 6 mg given intravenously, followedby one or two 6-mg boluses if necessary, iseffective and safe for acute treatment.A 5-mg bolus of verapamil (isoptin) , followed byone or two additional 5-mg boluses 10 min apartif the initial dose does not convert thearrhythmia
A 53 year old man with Ischaemic Heart Disease.
Wolf-Parkinson-White syndrome•short PR interval, less than 3 small squares (120 ms)•slurred upstroke to the QRS indicating pre-excitation (delta wave)•broad QRS•secondary ST and T wave changes Localising the accessory pathwayAn accessory pathway, bundle of Kent, exists between atria and ventricles and causesearly depolarisation of the ventricle. The location of the pathway may be deduced as follows:- LOCATION V1 V2 QRS axisleft posteroseptal (type A) +ve +ve leftright lateral (type B) -ve -ve leftleft lateral (type C) +ve +ve inferior (90 degrees)right posteroseptal -ve -ve leftanteroseptal -ve -ve normal
PSVT Due to Accessory Pathways (The Wolff-Parkinson-White Syndrome)
atrial fibrillation:Duration- Paroxysmal Minutes/hours- Short-lasting Seconds --<1 hour- Long-lasting >1 hour; -- < 48 hours- Persistent Two days -- weeks- Permanent (Chronic) Months / years
A woman with loud first heart sound and mid-diastolic murmur.
Treatment of Atrial FibrillationPharmacologic Management of Patients with RecurrentPersistent or Permanent AF:- Recurrent Persistent AF:A) Minimal or no symptoms: Anticoagulation and ratecontrol as needed.B) Disabling symptoms in AF:1- Anticoagulation and rate control2- Antiarrhythmic drug therapy3- Electrical cardioversion as needed, continueanticoagulation as needed and therapy to maintain sinusrhythm- Permanent AF: Anticoagulation and rate control asneeded.
Anticoagulation of Patients with AtrialFibrillation: IndicationsRheumatic mitral valve disease with recurrent orchronic atrial fibrillation.Dilated cardiomyopathy with recurrent persistent orchronic atrial fibrillation.Prosthetic valves.Prior to (>3 weeks) elective cardioversion ofpersistent or chronic atrial fibrillation, and also for 3weeks after cardioversion (because of atrialstunning).Coronary heart disease or hypertensive heart diseasewith recurrent persistent or chronic atrial fibrillation
Treatment of Cardiac Arrhythmias with CatheterAblative TechniquesRadiofrequency ablation destroys tissue bycontrolled heat production. Catheter ablation isused to treat patients with four majortachyarrhythmias:atrial flutter/fibrillation, AV nodal reentry,accessory pathways and ventricular tachycardia.