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Lo primero la estabilidad del paciente TCA. In the discussions that follow, patients are categorized as follows: Stable — This refers to a patient showing no evidence of hemodynamic compromise despite a sustained rapid heart rate. Such patients should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration. The presence of hemodynamic stability should not be regarded as diagnostic of SVT [4,10].

Misdiagnosis of VT as SVT based upon hemodynamic stability is a common error that can lead to inappropriate and potentially dangerous cardioverison. See “Pharmacologic interventions” below and see electriica diagnosis” below [3,4].

Unstable — This term refers to a patient with evidence of hemodynamic compromise, but who remains awake with a discernible pulse. In this setting, emergent synchronized cardioversion is the treatment of choice regardless of the mechanism of the arrhythmia.

See “Unstable patient” below. Findings consistent with hemodynamic instability requiring urgent cardioversion include hypotension, angina,altered level of consciousness, and heart failure. Patients who become unresponsive or pulseless are considered to have a cardiac arrest and are treated according to standard resuscitation algorithms. See “Overview of advanced cardiovascular life support in adults” and see “Overview of basic cardiovascular life support in adults”.

History of heart disease — The presence of structural heart disease, especially sincgonizada heart disease and a sincroniizada MI, strongly suggests VT as an etiology [4,7]. It is also important to establish whether a cardiac arrhythmia has occurred in the past and, if so, whether the patient is aware of the etiology. Patients are instructed to carry identification cards providing information about sjncronizada devices, which can facilitate device interrogation.

More importantly, the presence of an ICD implies that the patient is known to have an increased risk of ventricular tachyarrhythmias and carduoversion strongly but does not prove that the patient’s WCT is VT. See “General principles of the implantable cardioverter-defibrillator”.

Symptoms — Symptoms are not useful in determining the diagnosis, but they are important as an indicator of the severity of hemodynamic compromise. Symptoms are primarily due to the elevated heart rate, associated heart disease, and the presence of left ventricular dysfunction [4,6,7]. Some patients with a WCT have few or no symptoms palpitations, lightheadedness, diaphoresiswhile others have severe manifestations including chest pain or angina, syncope, shock, seizures, and cardiac arrest [6].

Age — A WCT in a patient over the age of 35 years is likely to be VT positive predictive value 85 percent in one series [11]. SVT is more likely in younger patients positive predictive value 70 percent. However, VT must be considered in younger patients, particularly those with a family history of ventricular arrhythmias or premature sudden cardiac death. Duration of the tachycardia — SVT is more likely if the tachycardia has recurred over a period of more than three years [6].

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The first occurrence of the tachycardia after an MI strongly implies VT [7]. Ventricular Pared ventricular lateral libre…. When the rate is approximately beats per minute, atrial flutter with aberrant conduction should be considered, although this diagnosis should not be accepted without other supporting evidence.

Regularity — VT is generally regular, although slight variation in the RR intervals is sometimes seen. Cardioverskon the onset of the arrhythmia is available for analysis, a period of irregularity “warm-up phenomenon”suggests VT. More marked irregularity of RR intervals occurs in polymorphic VT and in atrial fibrillation AF elecrtica aberrant conduction. When the arrhythmia arises in the lateral free wall of the ventricle sequential activation of the ventricles occurs resulting in a very wide QRS.

The QRS complex will be smaller when the VT has its origin in or close to the interventricular septum. Of course other factors also play a role in the QRS width during VT, such as scar tissue after myocardial infarctionventricular hypertrophy, and muscular disarray as in hypertrophic cardiomyopathy.

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It is of interest that a QRS width of more than 0. Of course, QRS width is not helpful in cardioersion VT from a tachycardia with AV conduction over an accessory AV pathway because such a pathway inserts into the ventricle leading to eccentric ventricular activation and a cxrdioversion QRS complex fig 6. BRHH preexistente ancianos con fibrosis sist. An antidromic circus movement tachycardia with AV conduction over a right sided accessory pathway.

The insertion of the accessory pathway in the free wall of the right ventricle results in sequential right to left ventricular activation and a wide QRS complex.

Alta probabilidad de TV Solo puede explicarse: On the left sinus rhythm is present with a very wide QRS because of anterolateral myocardial sincromizada and pronounced delay in left ventricular activation. On the right a VT arising on the right side of electfica interventricular septum results in more simultaneous activation of the right and left ventricle than during sinus rhythm and therefore a smaller QRS complex. As shown in fig 11, a very wide QRS is present during sinus rhythm because of sequential activation of first the right and then the left ventricle.

During tachycardia the QRS is more narrow. Eje muy negativo QRS axis in the frontal plane The QRS axis is not only important for the differentiation of the broad QRS tachycardia but also to identify its site of origin and aetiology.

As shown in fig 7, a VT origin in the apical part of the ventricle has a superior axis to the left of An inferior axis is present when the VT has an origin in the basal area of the ventricle. This does not hold for an LBBB shaped tachycardia. Puede existir y no ser obvia en ECG. Atrioventricular dissociation may be diagnosed by a changeable pulse pressure, irregular canon A waves in the jugular veins and a variable first heart sound. In the presence of AV dissociation, one may also observe fusion beats which may result from the fusion of a P wave conducted to the ventricles.

An atrial rate that is faster than the ventricular rate is seen with some SVTs, such as atrial flutter or an atrial tachycardia with 2: In these settings, however, there is a consistent relationship between the P waves and the QRS complexes, so there is not true AV dissociation.

While the presence of AV dissociation largely establishes VT as the diagnosis, its absence is not as helpful for two reasons: AV dissociation may be present but not obvious on the ECG. In some cases of VT, the ventricular impulses conduct backwards through the AV node and capture slncronizada atrium referred to as retrograde conductionpreventing AV dissociation [21]. One to one ventriculo-atrial conduction during VT.

Left panel VT; right panel same patient during sinus rhythm. The following findings are helpful in establishing the presence of AV dissociation. If P waves are not evident on the surface ECG, direct recordings of atrial activity eg, with an esophageal lead or an intracardiac catheter can reveal AV dissociation [22]. The resulting QRS complex has a morphology intermediate between that of a sinus beat and a purely ventricular complex show ECG 9. The term “capture beat” implies that the normal conduction system has momentarily “captured” control of ventricular activation from the VT focus.

Fusion crdioversion and capture beats are more commonly seen when the tachycardia rate is slower. Sudden narrowing of a QRS complex during VT may also be the result of a premature ventricular depolarisation arising in the ventricle in which the tachycardia originates, or it may occur when retrograde conduction during VT produces a ventricular echo beat leading to fusion with the VT QRS complex.

It may occur in AV junctional tachycardia with BBB after cardiac surgery or during digitalis intoxication. TV Eje izquierdo frontal V6 Marriott6 described that dincronizada RBBB shaped tachycardia, presence of a qR or R complex in lead V1 strongly argued for a ventricular origin of the tachycardia, while a three phasic RSR pattern suggested a supraventricular origin.

When in V6 the R: If the axis is inferiorly directed, lead V6 often shows an R: As described in the text, lead V1 during LBBB clearly shows signs pointing to a supraventricular origin of the tachycardia. Figure 12 gives an example of QR complexes during VT in patients with an anterior panel A and an old inferior myocardial infarction panel B.


cardioversion electrica sincronizada pdf creator

As shown by the accompanying tracing, during sinus rhythm anterior wall myocardial infarction is present in the left panel and inferior wall myocardial infarction in the right one. If all precordial leads are predominantly positive, the differential diagnosis is an xardioversion tachycardia using a left sided accessory pathway or a VT.

Negative concordancy is diagnostic for a VT arising in the apical area of the heart fig Positive concordancy means that in the horizontal electriva ventricular activation starts left posteriorly.

This can be found either in VT originating in the left posterior wall or during tachycardias using a left posterior accessory AV pathway for AV conduction fig The left panel shows a VT arising in the apical area of the left ventricle resulting in negative concordancy of all precordial leads. In the right panel ventricular activation starts in the left posterior area, resulting in positive concordancy of all precordial leads.


Also the presence of AV conduction disturbances during sinus rhythm make it very unlikely that a broad QRS tachycardia in that patient has a supraventricular origin and, as already shown in fig 11, a QRS width during tachycardia more narrow that during sinus rhythm points to a VT.

The first criterion is the presence of a positive and dominant R wave in lead aVR, and the second is based on the vi: The rationale for these criteria is eminently reasonable. A QRS axis that is deviated to the right superior quadrant has long been recognized as being caused by VT, and this phenomenon is similar to an R wave in lead aVR. SVT not associated with structural cardiac disease or drug presence, for example, would be expected to show rapid initial forces and delayed mid-terminal forces.

In this paper, Vereckei et al. We recently reported an ECG algorithm for differential diagnosis of regular wide QRS complex tachycardias that was superior to the Brugada algorithm. The purpose of this study was to further simplify the algorithm by omitting the complicated morphologic criteria and restricting the analysis to lead aVR.

In this study, wide QRS complex tachycardias [ ventricular tachycardias VTssupraventricular tachycardias SVTs20 preexcited tachycardias] from patients with proven diagnoses were prospectively analyzed by two of the authors blinded to the diagnosis.

When any of criteria 1 to 3 was present, VT was diagnosed; when absent, the next criterion was analyzed. The simplified aVR algorithm classified wide QRS complex tachycardias with the same accuracy as standard criteria and our previous algorithm and was superior to the Brugada algorithm.

Muesca en descenso inicial del QRS neg. The QRS complexes are not preceded by P waves. The origin of the QRS rhythm may be in the AV junction, with associated intraventricular aberration, or in fascicular or ventricular tissue. In the setting of AMI, the latter is more likely.

These notches might be P waves, or part of the QRS complexes themselves. If they are P waves, they occur in 1: Careful measurement of the QRS duration in the leads in which it is clearest indicates that the notches are in fact part of the QRS complexes and not P waves; no underlying atrial rhythm is discerned.

The QRS complexes have an LBBB pattern, but because ventricular depolarization may not be occurring over the normal AV node His-Purkinje pathway, definitive statements about underlying intraventricular conduction delay cannot be made.

A diagnosis of myocardial ischemia or infarction cannot be made with certainty in the presence of a left intraventricular conduction delay. In the setting of AMI, this rhythm could indicate either reperfusion elevtrica reperfusion injury.