Rarely, pulmonary edema may occur as a result of left atrial standstill or LV dysfunction after cardioversion in patients with longstanding AF. The two most common potentially life-threatening complications associated with cardioversion and defibrillation are arrhythmia and thromboembolism. Arrhythmias include sinus tachycardia, non-sustained VT, bradycardia and occasionally complete heart block that may require temporary cardiac pacing.
Clinically significant VT or VF may also occur infrequently. Previous studies in patients with atrial fibrillation have reported a post cardioversion stroke risk of 1. Much of these studies are retrospective analyses of data from emergency room visits and their results have not been reproduced in the ICU setting. The benefits of cardioversion in unstable AF outweighs the risk of clot embolization and therefore, urgent synchronized cardioversion should not be delayed in these patients.
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Enable Autosuggest. You have successfully created a MyAccess Profile for alertsuccessName. Home Books Critical Care. Previous Chapter. Next Chapter. Gupta R. Gupta, Rohit R. Cardioversion and Defibrillation. Oropello J. John M. Oropello, et al. Critical Care. McGraw Hill;. Accessed November 12, Cardioversion and defibrillation. McGraw Hill. Download citation file: RIS Zotero.
Reference Manager. Autosuggest Results. Download Section PDF. Table Graphic Jump Location Table 92—1 Initial energy requirements commonly used during cardioversion. View Table Download. Figure 92—1 Placement of the pads in an A anterolateral configuration and B anteroposterior configuration. Figure 92—2 Attach cables to ensure tight connection between electrode pads and the cardioverter. Figure 92—3 Use the Energy Select button to choose the energy level delivered during the cardioversion.
Figure 92—4 Use the Charge button to charge the cardioverter. Artucio H, Pereira M. Cardiac arrhythmias in critically ill patients: epidemiologic study. Crit Care Med. Professional Reference articles are designed for health professionals to use. You may find the Atrial Fibrillation article more useful, or one of our other health articles. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently.
The aim in both is to deliver electrical energy to the heart to stun the heart momentarily and thus allow a normal sinus rhythm to kick in via the heart's normal pacemaker, ie the sinoatrial node. This article will discuss defibrillation and cardioversion. See also separate Implantable Cardioverter Defibrillators article.
They applied electrical shocks and discovered that small shocks put the dogs' hearts into VF and this was successfully reversed with a larger shock. It was first used in humans by Claude Beck, a cardiothoracic surgeon - on a boy aged 14 years who was undergoing cardiothoracic surgery for congenital heart disease.
Electrodes were placed across the open heart. Closed chest defibrillation was not implemented until the s in Russia. But it was not until that Bernard Lown designed the modern-day monophasic defibrillator. This is based on the charging of capacitors and then delivering of a shock by paddles over a few milliseconds. In the s the biphasic waveform was discovered.
In monomorphic and polymorphic vt which one should be treated with synchronised cardioversion? And why? Monomorphic ventricular tachycardia is treated with synchronized cardioversion. The old defib machines particularly the monophasic ones used to take so long to charge up and then sync that there was too much of a delay in treating pulseless VT.
That is not the case anymore. It is well established that delivering a shock on the T-wave rather than the R-wave can cause VF. This is the basis of synchronised shocks. Modern defib machines are quick to charge, have sync buttons and we can monitor the ecg through the pads. Why not use synchronisation for all patients with VT, regardless of whether a pulse can be detected? I agree that our ability to detect a pulse should not impact the electrical treatment of VT. That being said, both synchronize cardioversion and defibrillation have a fairly high success rate for conversion of VT.
I have not seen a good rationale for continuing with no synchronization for pulseless VT. In these situations, a physician does have the discretion to attempt synchronization. Healthcare providers are allowed to tailor their actions using their discretion for the best outcome. Once you deliver unsynch shock to VT is there a chance for conversion to VF? If so why should we create a risk of VF not trying to synchronize the shock in any VT? Pulse has nothing to do, I presume, as you may feel the pulse while I can not… Is the patient pulseless?
The research and clinical data from the past 70 years indicates that the most effective intervention for pulseless ventricular tachycardia is and unsynchronized shock. This is what should be performed if no pulse is felt and a patient is unresponsive. After the unsynchronized shock, chest compressions should begin immediately. Initial dose is Side effects are slurred speech, altered levels of consciousness, seizures and bradycardia.
Magnesium can be used for polymorphic Vtach associated with QT prolongation, also called torsades de pointes. Dose is mg IV over 15 minutes. Side effects are hypotension, CNS toxicity, respiratory depression. Follow levels and watch closely with concomitant renal dysfunction. Vtach response to therapy depends on underlying etiology. Key to treatment past antiarrhythmics and electricity will be identifying possible causes defined in pathophysiology section. If front-line arrhythmia therapy fails or clinical situation deteriorates, reconsider diagnosis.
Reevaluate EKG, clinical history and presentation. Seek expert help. The vast majority of adult cardiac arrests from Vfib and pulseless Vtach are secondary to myocardial ischemia, around , people per year. These arrhythmias are the most common cause of death in acute myocardial infarction. Primary Vfib not associated with an MI needs evaluation by an electrophysiologist. Vtach occurs in areas of scar from prior MI, the risk of development depending on severity of myocardial necrosis, LV dysfunction and the degree of septal involvement.
Thus stable Vtach is more likely from an arrhythmogenic focus in an old scar. Therapy should be focused on underlying hypoxia, electrolytes, etc. Other possible causes of monomorphic Vtach include: dilated cardiomyopathy, hypertrophic cardiomyopathy, myocarditis, RV dysplasia, drug toxicity and electrolyte abnormalities. Polymorphic Vtach in the setting of a normal QT is usually secondary to acute coronary ischemia or myocardial infarction.
Outside of congenital syndromes such as long QT syndrome, polymorphic Vtach from prolonged QT occurs most frequently following exposure to a QT-prolonging drug. Risk factors for torsades are female gender, hypokalemia, bradycardia, recent conversion from atrial fibrillation especially with a QT0prolonging drug, CHF, digitalis, baseline QT prolongation, subclinical QT syndrome or severe hypomagnesemia.
For Vfib arrest, high-quality CPR and defibrillation have been proven to increase survival to hospital disharge. Vascular access, drug delivery, advanced airway should not cause significant disruptions in CPR or delay defrbrillation. Amiodarone is the first-line antiarrhythmic during cardiac arrest, as it has been shown to improve return to circulation.
Two observational studies have shown that magnesium can terminate torsades de pointes, it is not likely to be effective in terminating irregular or polymorphic Vtach with a normal QT interval. For stable Vtach, IV antiarrhythmic drugs or elective cardioversion is recommended. Lidocaine has been found to be less effective than amiodarone, sotalol or procainamide. Procainamide and sotalol should be avoided with QT prolongation. Procainamide should be avoided in CHF.
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