Can you cardiovert ventricular tachycardia




















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.

If VF is present when a rhythm check is performed after 2 min. Stable Vtach can be managed pharmacologically. Vfib is rapid totally incoordinate contraction of ventricular fibers; the EKG shows chaotic electrical activity and clinically the patient has no pulse. Vtach is defined by QRS greater than or equal to. There are three clinical types: pulseless, hemodynamically unstable and hemodynamically stable.

If there is any doubt of polymorphic versus monomorphic Vtach in the hemodynamically unstable patient, treat like Vfib. If Vtach or Vfib, prepare for defibrillation. If pulse is present, attach EKG or defibrillator and evaluate rhythm. If patient is unstable and not polymorphic Vtach, prepare for synchronized cardoversion. Determine whether patients has pulse or not. As action to restore circulation begins, think of what caused the arrest. Vfib is defined by totally incoordinate contraction of ventricular fibers, reflected on EKG by chaotic electrical activity.

Wide complex tachycardia other than pulseless Vtach and Vfib needs to be separated into stable or unstable; regular or irregular.

Hemodynamic instability examples include: altered mental status, ischemic chest discomfort, acute heart failure, respiratory distress, hypotension or other signs of shock. Wide complex tachycardia is defined as a QRS greater than. Vtach diagnosis is supported by evidence of AV dissociation, wide complexes greater than ms, and axis is positive or negative in all leads. Monomorphic Vtach has one morphology of QRS complexes. Polymorphic Vtach has progressive changes in QRS complex, which means multiple morphologies.

Polymorphic Vtach with a prolonged QT greater than msec when heart rate corrected is called torsades de pointes Figure 1. Vfib is easily diagnosed by EKG; just do not forget to check EKG leads during the code to be sure they do not come unattached. A wide complex tachycardia that is regular could be Vtach, SVT with aberrancy, pre-excited tachycardia or a v-paced rhythm.

A wide complex tachycardia that is irregular may be atrial fibrillation with aberrancy, pre-excited atrial fibrillation, polymorphic vtach or torsades de pointes.

If the etiology of the rhythm cannot be determined, the rate is regular and the QRS is monomorphic, then adenosine mg IV can be given. If SVT it will convert or slow; if no response then it is Vtach. Always have patient attached to defibrillator when giving adenosine in this clinical scenario. Do not give adenosine to unstable patients or those with irregular or regular polymorphic wide complex tachycardias. In these scenarios adenosine could lead to Vfib. Biphasic defibrillation use to joules; it is acceptable to use maximum dose if unsure, For monophasic defibrillators use joules.

After defibrillation continue CPR for 2 minutes before checking pulse. If no return to circulation, defibrillate again and check pulse in 2 minutes. In cases such as in VF or pulseless VT, CPR should not be delayed and should be initiated immediately while preparing for defibrillation. The AHA Guidelines for cardiopulmonary resuscitation CPR and emergency cardiovascular care ECC recommends high quality CPR to be initiated for at least 90 to seconds while the defibrillator pads and electrodes are being applied and before first defibrillation is attempted.

It is believed that during VF, the myocardium is being depleted of oxygen and energy and that delivering CPR during this crucial period will provide the needed oxygen and energy, as well as increase the likelihood of terminating VF during defibrillation and rapid return of spontaneous circulation. Electrolyte imbalances such as hypocalcemia, hypokalemia and hypomagnesemia should also be corrected to improve successful cardioversion.

The following are basic steps for using the cardioverter:. Most defibrillator brands are multifunctional and can be used as an automated external defibrillator AED , manual defibrillator, external pacer or for ECG monitoring. Make sure that the device is set to defibrillator mode. Once connected, the monitor will display the ECG tracing and the heart rate. The device automatically returns to asynchronous mode after each synchronized discharge.

A charge tone indicates that the charge is complete to the selected energy level Figure 92—4. After the shock is delivered, the energy for each subsequent shock is automatically selected based on the energy level configured on the set-up.

Use the Energy Select button to choose the energy level delivered during the cardioversion. These can be grouped as patient characteristics such as body habitus, device characteristics including paddle size, waveform morphology and iatrogenic factors including administration of medications and ventilator support. Electric shocks used in cardioversion and defibrillation are quantified by the amount of energy delivered. While this allows for the standardization of shocks delivered, it is important to understand that the determinant of an adequate shock is not the energy itself but the amount of electrical current that travels across the heart depolarizing the myocardium.

This resistance, termed as thoracic impedance, is determined by the electrode-to-skin interface, electrode pressure, body habitus and the phase of ventilation. Decreasing the interface between the skin and the paddle by placing more pressure on the paddles, applying adhesive or more conductive gel as well as delivering shocks during expiration decreases thoracic impedance and increases the effectiveness of cardioversion and defibrillation.

Hairs should also be shaved off the chest if necessary to facilitate attachment of electrode pads to the skin. Pad size is also an important determinant of transthoracic flow during delivery of shocks.

A paddle or pad size with larger surface area has been associated with less thoracic resistance and less chances of myocardial injury. Observational studies have shown that persistent AF may be more easily converted using a hand-held paddle and the improved electrode-to-skin contact and reduced thoracic impedance are likely contributing to the higher success rate of cardioversion.

There has been ongoing debate about the relative impact of the positioning of the electrodes on the outcome of the cardioversion attempt. Consequently we do not recommend a particular position for electrode placement over another. A final point should be made about the use of antiarrhythmic drugs prior to attempted cardioversion.

While evidence is limited, in patients who have been pretreated with amiodarone , ibutilide , propafenone or sotalol , the restoration of a sinus rhythm from AF required less electrical energy, fewer attempts and lower number of recurrences. Among the various cardiac pathologies complicating pregnancy, arrhythmias are the most common.

Often diagnosed for the first time during pregnancy, tachyarrhythmias are the commonest form of arrhythmias reported during pregnancy. Cardioversion and defibrillation during pregnancy is relatively safe without documented adverse effects to the fetus.

However, antepartum fetal monitoring is recommended to monitor fetal heart rate during the procedure. Special consideration of the duration of pregnancy should be made while choosing drugs used for sedation pre-procedure, for example, avoid midazolam.

Since the implantation of the first ICD in , there has been a great increase in the use of these instruments and their presence in ICU patients. Occasionally patients continue to have unstable tachyarrhythmias despite having a functioning device. In certain instances, the ICD can be successfully reprogrammed to deliver the shock internally or implement tachycardia-pacing strategies for managing tachyarrhythmia.

The application of electrical current during synchronized and unsynchronized cardioversion in patients with an ICD or permanent pacemaker can potentially cause damage to the ICD circuit and cause malfunction of these devices. However, hemodynamically unstable tachyarrhythmias that are not being controlled by the implanted device need to be treated without hesitation in a manner similar to any other patient in the ICU.

As a strategy for minimizing risk of device damage, it is recommended to place the pads at least 12 cm away from the pulse generator and to use the anteroposterior positioning of electrodes.

All ICDs and permanent pacemakers should be interrogated after cardioversion is performed to ensure the proper functioning of these devices. An initial study from revealed a significant increase in the incidence of serious postcardioversion ventricular ectopy in patients that had ECG evidence of digitalis toxicity precardioversion.

Subsequent studies have confirmed that sustained ventricular ectopy post cardioversion is exceedingly rare and tends to occur with higher energy cardioversion along with other concomitant factors such as hypokalemia. As with all tachyarrhythmias it is important to identify and treat the underlying cause. If cardioversion is deemed necessary it should be carried out starting with a lower energy level and ensuring the correction of any electrolyte abnormalities.

Complications of cardioversion include skin burns, transient hypotension commonly from sedation , and EKG changes such as nonspecific ST-T wave changes or transient ST segment elevation.

High-energy shocks may also result in myocardial necrosis, which may present as a small rise in cardiac enzymes. Myocardial dysfunction may also occur due to myocardial stunning and is usually related to ischemia during cardiac arrest. This complication usually improves in 24 to 48 hours post resuscitation. 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. In these cases, identifying primary causation, performing good CPR, and administering epinephrine are the only tools you have to resuscitate the patient.

Shockable rhythms are rhythms that are caused by an aberration in the electrical conduction system of the heart. Ventricular tachycardia v-tach typically responds well to defibrillation. This rhythm usually appears on the monitor as a wide, regular, and very rapid rhythm. Ventricular tachycardia is a poorly perfusing rhythm; patients may present with or without a pulse.

Multiple shocks may be needed, but good compressions and adequate ventilation are also important.



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