ECG in Ventricular arrhythmias Dr Mostafa Hekmat CardiologistElectrophysiologist.
-
Upload
steve-delaney -
Category
Documents
-
view
226 -
download
0
Transcript of ECG in Ventricular arrhythmias Dr Mostafa Hekmat CardiologistElectrophysiologist.
ECG in Ventricular
arrhythmiasDr Mostafa Hekmat
Cardiologist
Electrophysiologist
Dr Hekmat 2
A look at ventricular arrhythmias
•Ventricular arrhythmias originate in the ventricles below the bundle of His.
•They occur when electrical impulsesdepolarize 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 mayshow 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 duringcell 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 0.12 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 Mostafa Hekmat 15
Dr Hekmat 16
Dr Hekmat 17
Dr Hekmat 18
Dr Mostafa Hekmat 19
An interpolated PVC
Dr Hekmat 20
Dr Mostafa Hekmat 21
Multiform
Dr Hekmat 22
Couplet
Dr Hekmat 23
Bigeminy
Dr Hekmat 24
Dr Hekmat 25
Dr Mostafa 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 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 lastingfewer 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 withhypotension 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 Mostafa 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 Hekmat 43
Left Septal VT
Dr Mostafa 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 Hekmat 45
RVOT VT
Dr Mostafa 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
Dr Mostafa Hekmat 48
Supraventricular arrhythmiawith 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
• 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 Hekmat 50
Dr Hekmat 51
Dr Hekmat 52
Dr Hekmat 53
Dr Hekmat 54
Dr Hekmat 55
56
Treatment
Dr Hekmat
Dr Mostafa Hekmat 57
Treatment
•PVCs, even in the setting of an acute MI, need not be treated unless they directly contribute to hemodynamic compromise
Dr Hekmat 58
Treatment
•Any wide QRS complex tachycardia should be treated as ventricular tachycardia until definitive evidence is found to establish another diagnosis
Dr Mostafa 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 Hekmat 60