0 ecg arrhythmia for medical students samir rafla
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This document provides an overview of cardiac arrhythmias for medical students. It begins with an introduction to conduction pathways and ECG patterns. It then classifies arrhythmias as rapid and regular, rapid and irregular, or slow and regular. Specific arrhythmias are defined and their causes discussed, including sinus tachycardia, sinus bradycardia, supraventricular tachycardias, atrial fibrillation, Wolff-Parkinson-White syndrome, atrial flutter, ventricular tachycardia, heart block, and sudden cardiac death. Treatment options are also reviewed for many of the arrhythmias.
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Semelhante a 0 ecg arrhythmia for medical students samir rafla
Semelhante a 0 ecg arrhythmia for medical students samir rafla (20)
Mais de Alexandria University, Egypt
Mais de Alexandria University, Egypt (20)
0 ecg arrhythmia for medical students samir rafla
- 1. Arrhythmia for Medical Students Samir Rafla, FACC, FESC Prof. of Cardiology Alexandria University
- 2. The pathways of Conduction
- 3. Normal ECG
- 5. Classification of arrhythmia: - Rapid, regular. Sinus tachycardia, supraventricular tachycardia, atrial flutter, ventricular tachycardia. - Rapid, irregular. Sinus arrhythmia, multiple ectopic beats whether atrial or ventricular, atrial fibrillation. - Slow, regular. Sinus bradycardia, nodal rhythm, complete heart block.
- 6. Sinus tachycardia Cardiac impulses arise in the sinus node at a rate more than 100/min. 4 Etiology: A- Physiological: Infancy, childhood, exercise and excitement. B- Pharmacological: Sympathomimetic drugs such as epinephrine and isoproterenol. Parasympatholytic drugs such as atropine. Thyroid hormones, nicotine, caffeine, alcohol. C- Pathological: Fever, hypotension, heart failure, pulmonary embolism, hyperkinetic circulatory states as anemia.
- 7. A 34 year old woman with asthma
- 8. Sinus Bradycardia Cardiac impulses arise in the sinus node at a rate less than 60/min. Etiology: A- Physiologic: Athletes, sleep, and carotid sinus compression. B- Pharmacologic: Digitalis, propranolol, verapamil and diltiazem. C- Pathologic: Convalescence from infections, hypothyroidism, obstructive jaundice, rapid rise of the intracranial tension, hypothermia and myocardial infarction (particularly inferior wall infarction)
- 9. SUPRAVENTRICULAR TACHYARRHYTHMIAS SVTs may be separated into three groups based on duration: brief paroxysms, persistent, and chronic (permanent). Arrhythmias that are paroxysmal in onset and offset (e.g. paroxysmal SVT due to AV nodal reentry or WPW syndrome, paroxysmal atrial fibrillation, paroxysmal atrial flutter) tend to be recurrent and of short duration
- 10. Supraventricular tachyarrhythmias include: atrial tachycardia, atrial flutter, atrial fibrillation and AV tachycardias.
- 11. PSVT
- 12. Management of PSVT Due to AV Nodal Reentry The acute attack: Vagal maneuvers serve as the first line of therapy. Simple procedures to terminate paroxysmal SVT - Carotid sinus massage: If effective the rhythm is abruptly stopped; occasionally only moderate slowing occurs - Cold water splash on face. - Performance of Valsalva's maneuver (often effective).
- 13. Management of PSVT Due to AV Nodal Reentry Intravenous adenosine, Ca channel blockers (verapamil), digoxin or B-blockers are the choices for managing the acute episodes. Adenosine, 6 mg given intravenously, followed by one or two 6-mg boluses if necessary, is effective and safe for acute treatment. A 5-mg bolus of verapamil (isoptin) , followed by one or two additional 5-mg boluses 10 min apart if the initial dose does not convert the arrhythmia
- 14. SVT
- 15. A 53 year old man with Ischaemic Heart Disease.
- 16. 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
- 17. PSVT Due to Accessory Pathways (The Wolff-Parkinson-White Syndrome)
- 18. 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
- 19. Causes of atrial fibrillation With structural heart disease - Rheumatic mitral valve disease - Ischemic heart disease - Hypertension - Cardiomyopathy: Dilated, Hypertrophic - Atrial septal defect, - Constrictive pericarditis, Myocarditis Without structural heart disease - Alcohol. Thyrotoxicosis - Acute pericarditis. Pulmonary embolism - Sick sinus syndrome, Lone atrial fibrillation
- 20. A woman with loud first heart sound and mid-diastolic murmur.
- 21. Treatment of Atrial Fibrillation Pharmacologic Management of Patients with Recurrent Persistent or Permanent AF: - Recurrent Persistent AF: A) Minimal or no symptoms: Anticoagulation and rate control as needed. B) Disabling symptoms in AF: 1- Anticoagulation and rate control 2- Antiarrhythmic drug therapy 3- Electrical cardioversion as needed, continue anticoagulation as needed and therapy to maintain sinus rhythm - Permanent AF: Anticoagulation and rate control as needed.
- 24. 24
- 25. AF management
- 26. Anticoagulation of Patients with Atrial Fibrillation: Indications Rheumatic mitral valve disease with recurrent or chronic atrial fibrillation. Dilated cardiomyopathy with recurrent persistent or chronic atrial fibrillation. Prosthetic valves. Prior to (>3 weeks) elective cardioversion of persistent or chronic atrial fibrillation, and also for 3 weeks after cardioversion (because of atrial stunning). Coronary heart disease or hypertensive heart disease with recurrent persistent or chronic atrial fibrillation
- 27. Atrial Flutter
- 28. Treatment of Cardiac Arrhythmias with Catheter Ablative Techniques Radiofrequency ablation destroys tissue by controlled heat production. Catheter ablation is used to treat patients with four major tachyarrhythmias: atrial flutter/fibrillation, AV nodal reentry, accessory pathways and ventricular tachycardia.
- 29. A 76 year old man with SOB
- 30. A 60 year old woman with HTN
- 31. A 68 year old women on Digoxin complaining of fatigue
- 32. A 57 year old woman with palpitations
- 33. A woman with Romano-Ward Syndrome
- 34. QTc Normal QTc • Men < 0.43 – borderline o.43-0.45 – prolonged >0.45 • Women < 0.43 – borderline o.43-0.47 – prolonged >0.47
- 35. A 50 year old man with chest pain for 2-4 hours
- 38. A 45 year old women with palpitation and a history of CRF (Chronic Renal Failure)
- 39. A 69 year old man 2 weeks post IW MI
- 40. A 60 year old man with IHD
- 41. A 25 year old man with bouts of tachycardia
- 42. A 23 year old male with palpitations
- 43. AV HEART BLOCK
- 44. Mobitz type I (Wenckebach) block Mobitz Type II second degree heart block
- 46. A 73 year old woman with dizziness.
- 47. A 70 year old man with exercise intolerance.
- 48. An 82 year old lady with dizzy spells
- 49. Sudden Cardiac Death Definition: unexpected natural death due to cardiac cause within one hour from the onset of symptoms .
Notas do Editor
- 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.