Presentation is loading. Please wait.

Presentation is loading. Please wait.

ECG in Ventricular arrhythmias

Similar presentations

Presentation on theme: "ECG in Ventricular arrhythmias"— Presentation transcript:

1 ECG in Ventricular arrhythmias
Dr Mostafa Hekmat Cardiologist Electrophysiologist

2 A look at ventricular arrhythmias
Ventricular arrhythmias originate in the ventricles below the bundle of His. They occur when electrical impulses depolarize the myocardium using a different pathway from normal impulses Dr Hekmat

3 A look at ventricular arrhythmias
Ventricular arrhythmias appear on an ECG in characteristic ways. The QRS complex is wider than normal because of the prolonged conduction time through the ventricles Dr Hekmat

4 A look at ventricular arrhythmias
The T wave and the QRS complex deflect in opposite directions because of the difference in the action potential during ventricular depolarization and repolarization. P wave is absent because atrial depolarization doesn’t occur Dr Hekmat

5 No kick from the atria When electrical impulses are generated from the ventricles instead of the atria, atrial kick is lost Cardiac output decreases by as much as 30%. Patients with ventricular arrhythmias may show signs and symptoms of cardiac decompensation, including hypotension, angina, syncope, and respiratory distress. Dr Hekmat

6 Potential to kill Although ventricular arrhythmias may be benign, they’re potentially deadly because the ventricles are ultimately responsible for cardiac output. Rapid recognition and treatment of ventricular arrhythmias increases the chance for successful resuscitation Dr Hekmat

7 Premature ventricular contraction
A PVC is an ectopic beat that may occur in healthy people without causing problems. PVCs may occur singly, in clusters of two or more, or in repeating patterns, such as bigeminy or trigeminy When PVCs occur in patients with underlying heart disease, they may indicate impending lethal ventricular arrhythmias Dr Hekmat

8 Premature ventricular contraction
PVCs are usually caused by electrical irritability in the ventricular conduction system or muscle tissue. This irritability may be provoked by anything that disrupts normal electrolyte shifts during cell depolarization and repolarization Dr Hekmat

9 Premature ventricular contraction
Electrolyte imbalances, such as hypokalemia, hyperkalemia, hypomagnesemia, and hypocalcemia Metabolic acidosis Hypoxia Myocardial ischemia and infarction Drug intoxication, particularly cocaine, amphetamines, and tricyclic antidepressants Enlargement of the ventricular chambers Increased sympathetic stimulation Myocarditis Caffeine or alcohol ingestion Proarrhythmic effects of some antiarrhythmics Tobacco use. Dr Hekmat

10 Premature ventricular contraction
PVCs are significant for two reasons. 1, they can lead to more serious arrhythmias, such as ventricular tachycardia or ventricular fibrillation. The risk of developing a more serious arrhythmia increases in patients with ischemic or damaged hearts. 2,PVCs also decrease cardiac output, especially if the ectopic beats are frequent or sustained. Decreased cardiac output is caused by reduced ventricular diastolic filling time and a loss of atrial kick Dr Hekmat

11 Dr Hekmat

12 PVC PVCs look wide and bizarre and appear as early beats causing atrial and ventricular irregularity. The P wave is usually absent. Retrograde P waves may be stimulated by the PVC and cause distortion of the ST segment. The PR interval and QT interval aren’t measurable on a premature beat, QRS complex in the premature beat exceeds second. The T wave in the premature beat has a deflection opposite that of the QRS complex. Dr Hekmat

13 R-on-T When a PVC strikes on the downslope of the preceding normal T wave it can trigger more serious rhythm disturbances Because the cells haven’t fully repolarized, VT or VF can result Dr Hekmat

14 The pause that compensates
Interval between two normal sinus beats containing a PVC equals two normal sinus intervals. Dr Hekmat

15 Dr Mostafa Hekmat

16 Dr Hekmat

17 Dr Hekmat

18 Dr Hekmat

19 An interpolated PVC Dr Mostafa Hekmat

20 Dr Hekmat

21 Multiform Multiform PVCs. The normally conducted QRS complexes exhibit a left bundle branch block contour (arrowhead) and are followed by PVCs with three different morphologies. Dr Mostafa Hekmat

22 Couplet Dr Hekmat

23 Bigeminy Dr Hekmat

24 Dr Hekmat

25 Dr Hekmat

26 CLINICAL FEATURES The prevalence of premature complexes increases with
Age Male gender Hypokalemia PVCs are more frequent in the morning in patients after MI This circadian variation is absent in patients with severe left ventricular dysfunction. Dr Mostafa Hekmat

27 The importance of PVCs Depends on the clinical setting
In the absence of underlying heart disease, the presence of PVCs usually has no impact on longevity or limitation of activity Antiarrhythmic drugs are not indicated Patients should be reassured if they are symptomatic Dr Mostafa Hekmat

28 Identifying idioventricular rhythm
Dr Hekmat

29 Accelerated idioventricular rhythm
Dr Hekmat

30 Dr Hekmat

31 Torsades de pointes Dr Hekmat

32 Dr Hekmat

33 Torsades de pointes Is a special form of polymorphic ventricular tachycardia The rate is 150 to 250 beats/minute, usually with an irregular rhythm, and the QRS complexes are wide with changing amplitude. Dr Hekmat

34 Torsades de pointes This arrhythmia may be paroxysmal, starting and stopping suddenly, and may deteriorate into ventricular fibrillation Reversible causes Amiodarone, ibutilide, erythromycin, haloperidol, droperidol, and sotalol Myocardial ischemia and electrolyte abnormalities, such as hypokalemia, hypomagnesemia, and hypocalcemia Dr Hekmat

35 Ventricular fibrillation
Electrical activity in the ventricles Electrical impulses arise from many different foci. It produces no effective muscular contraction and no cardiac output. Dr Hekmat

36 Dr Hekmat

37 Ventricular tachycardia
Three or more PVCs occur in a row and the ventricular rate exceeds 100 beats/minute VT is an extremely unstable rhythm. It can occur in short, paroxysmal bursts lasting fewer than 30 seconds and causing few or no symptoms. Alternatively, it can be sustained, requiring immediate treatment to prevent death, even in patients initially able to maintain adequate cardiac output Dr Hekmat

38 Ventricular tachycardia
Conditions that can cause ventricular tachycardia include: MI Coronary artery disease Valvular heart disease Heart failure Cardiomyopathy Electrolyte imbalances such as hypokalemia Drug intoxication from digoxin (Lanoxin), procainamide, Quinidine, or Cocaine Proarrhythmic effects of some antiarrhythmics Dr Hekmat

39 Unpredictable V-tach A patient may be stable with a normal pulse and adequate hemodynamics or unstable with hypotension and no detectable pulse. Because of reduced ventricular filling time and the drop in cardiac output, the patient’s condition can quickly deteriorate to ventricular fibrillation and complete cardiac collapse Dr Hekmat

40 Ventricular tachycardia
The ventricular rate is usually rapid—100 to 250 beats/minute. The P wave is usually absent but may be obscured by the QRS complex. Retrograde P waves may be present. The QRS complex is wide and bizarre, usually with an increased amplitude and a duration of longer than 0.12 second. Dr Hekmat

41 Dr Hekmat

42 VT + RBBB (1) the QRS complex is monophasic or biphasic in V1, with an initial deflection different from that of the sinus-initiated QRS complex (2) the amplitude of the R wave in V1 exceeds the R′ (3) a small R and large S wave or a QS pattern in V6 may be present. Dr Mostafa Hekmat

43 Left Septal VT Dr Hekmat

44 VT + LBBB (1) the axis can be rightward, with negative deflections deeper in V1 than in V6, (2) a broad prolonged (more than 40 milliseconds) R wave in V1 (3) a small Q–large R wave or QS pattern in V6 can exist Dr Mostafa Hekmat

45 RVOT VT Dr Hekmat

46 VT QRS duration exceeding 140 milliseconds
In precordial leads with an RS pattern, the duration of the onset of the R to the nadir of the S exceeding 100 Fusion beat Capture beat AV dissociation has long been considered a hallmark of VT Retrograde VA conduction to the atria from ventricular beats occurs in at least 25% of patients Dr Mostafa Hekmat

47 Fusion and capture beats during VT
Fusion and capture beats during VT. The QRS complex is prolonged, and the R-R interval is regular except for occasional capture beats (C) that have a normal contour and are slightly premature. Complexes intermediate in contour represent fusion beats (F). Thus, even though atrial activity is not clearly apparent, AV dissociation is present during VT and produces intermittent capture and fusion beats. Dr Mostafa Hekmat

48 Supraventricular arrhythmia with aberrancy
(1) consistent onset of the tachycardia with a premature P wave (2) very short RP interval (0.1 sec) (3) QRS configuration the same as that occurring from known supraventricular conduction at similar rates (4) P wave and QRS rate and rhythm linked to suggest that ventricular activation depends on atrial discharge (an AV Wenckebach block) (5) slowing or termination of the tachycardia by vagal maneuvers Dr Mostafa Hekmat

49 The presence of a 2 : 1 VA block  VT Positive QRS complex in V1 - V6
A QRS complex in V1 - V6,  either all negative or all positive  favors a VT The presence of a 2 : 1 VA block  VT Positive QRS complex in V1 - V6 Can also occur from conduction over a left-sided accessory pathway. Supraventricular beats with aberration Triphasic pattern in V1 An initial vector of the abnormal complex similar to that of the normally conducted beats Wide QRS complex with long-short cycle sequence Dr Mostafa Hekmat

50 Dr Hekmat

51 Dr Hekmat

52 Dr Hekmat

53 Dr Hekmat

54 Dr Hekmat

55 Dr Hekmat

56 Treatment Dr Hekmat

57 Treatment PVCs, even in the setting of an acute MI, need not be treated unless they directly contribute to hemodynamic compromise Dr Mostafa Hekmat

58 Treatment Any wide QRS complex tachycardia should be treated as ventricular tachycardia until definitive evidence is found to establish another diagnosis Dr Hekmat

59 Treatment Beta blockers are often the first line of therapy.
If they are ineffective, class IC drugs seem particularly successful in suppressing PVCs, Flecainide and Moricizine have been shown to increase mortality in patients treated after MI Should be reserved for patients without coronary artery disease or LV dysfunction Amiodarone Should be reserved for highly symptomatic patients and those with structural heart disease. Dr Mostafa Hekmat

60 Dr Hekmat

Download ppt "ECG in Ventricular arrhythmias"

Similar presentations

Ads by Google