Ventricular tachycardia/fibrillation

If pulseless ventricular tachycardia/fibrillation develops, go to page 384 if PEA develops, go to page 385... 

On the other hand, a number of studies have shown that morphine and opioid peptides could have cardioprotective effects toward ischemic processes and may be able to reduce the size of infarct [72,73]. These effects seem to involve the activation of delta opioid receptors, the localization of which remains unknown. In addition, enkephalin-degrading enzyme inhibitors, such as acetorphan and, particularly, RB 101, have also been demonstrated to decrease the susceptibility to the arrhythmogenic action of epinephrine. Thus RB 101 completely prevented the ventricular tachycardia, fibrillation, and repetitive ventricular extrasystoles induced by epinephrine (Maslov et al., unpublished data). These effects were reversed by the selective delta antagonist ICI 174,864. 

The localization of adducts to the epicardial border zone suggested the possibility that IsoK/LG adducts contribute to cardiac arrhythmias. Ventricular tachycardia/fibrillation following myocardial infarction is a major cause of sudden cardiac death. Arrhythmias in ischemic myocardium arise from sodium channel blockade. Sodium channels are hypothesized to cycle between three conformational states a deactivated closed state, an activated open state, and an inactivated closed state. Upon depolarization, the deactivated state converts to the activated state and sodium current flows for a brief time before the channel enters the inactive state. The channel only converts from the inactive state to the deactivated state when the membrane repolarizes during the falling phase of the action potential. Changes in the ability to convert from the inactive to the deactivated state are critical to the initiation and perpetuation of arrhythmias. 

Cardiovascular Ventricular tachycardia/ fibrillation in an otherwise healthy 48-year-old woman who was taking no medications other than phentermine was attributed to sympathetic activation [103" ]. The cardiac safety concern of phentermine suggested by these authors has been debated [104"]. 

Both conditions predispose the patient to dangerous ventricular arrhythmias (Ventricular Tachycardia/Fibrillation and/or Torsades). 

Long QT syndromes can predispose patients to dangerous ventricular arrhythmias such as Ventricular Tachycardia/Fibrillation. 

Reentry mechanism Intranodal (AV node) reentry Extranodal reentry Reentrant tachyarrhythmia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation Conduction B/ocks ... 

The uses of the antiarrhythmic drug are given in the Summaiy Drug Table Antiarrhythmic Drug3. In general these drugp are used to prevent and treat cardiac arrhythmias, such as premature ventricular contractions (PVCs), ventricular tachycardia (VT), premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), atrial fibrillation, and atrial flutter. Some of the antiarrhythmic dru are used for other... 

Proarrhytlimic effects (worsening of the existing arrhythmia or causation of a new arrhythmia) may occur, such as severe ventricular tachycardia or ventricular fibrillation. It is often difficult to distinguish proarrhytlimic effects from the patient s preexisting arrhythmia. 

Figure 4.2 Epicardial ECG recorded from an isolated blood-perfused rat heart at the moment of reperfusion. The heart was made regionally ischaemic by occluding a snare around the left anterior descending coronary artery and, after 10 min, reperfused by releasing the snare. Note the rapid onset of ventricular tachycardia (VT) and its subsequent degeneration into ventricular fibrillation (VF). Reproduced with permission from Lawson (1993).

Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm... 

Treat polymorphic ventricular tachycardia (irregular rate and form) as ventricular fibrillation (see Table 1.9)... 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

TABLE 6-10. Etiologies of Ventricular Tachycardia and Ventricular Fibrillation... 

FIGURE 6-12. Decision algorithm for resuscitation of ventricular fibrillation or pulseless ventricular tachycardia. 

Implantable cardioverter-defibrillator (ICD) A device implanted into the heart transvenously with a generator implanted subcutaneously in the pectoral area that provides internal electrical cardioversion of ventricular tachycardia or defibriUation of ventricular fibrillation. 

AF, atrial fibrillation HF, heart failure 10, intraosseous PSVT, paroxysmal supraventricular tachycardia VF, ventricular fibrillation VT, ventricular tachycardia. 

FIGURE 6-2. Algorithm for the treatment of acute (top portion) paroxysmal supraventricular tachycardia and chronic prevention of recurrences (bottom portion). Note For empiric bridge therapy prior to radiofrequency ablation procedures, calcium channel blockers (or other atrioventricular [AV] nodal blockers) should not be used if the patient has AV reentry with an accessory pathway. (AAD, antiarrhythmic drugs AF, atrial fibrillation AP, accessory pathway AVN, atrioventricular nodal AVNRT, atrioventricular nodal reentrant tachycardia AVRT, atrioventricular reentrant tachycardia DCC, direct-current cardioversion ECG, electrocardiographic monitoring EPS, electrophysiologic studies PRN, as needed VT, ventricular tachycardia.)... 

Cardiopulmonary arrest in adults usually results from arrhythmias. The most common arrhythmias are ventricular fibrillation (VF) and pulseless ventricular tachycardia (PVT), often in patients after myocardial infarction (MI) or pulmonary embolism (PE). In children, cardiopulmonary arrest is often the terminal event of progressive shock or respiratory failure. 

CPR, cardiopulmonary resuscitation D5W, 5% dextrose in water PEA, pulseless electrical activity PVT, pulseless ventricular tachycardia ROSC, return of spontaneous circulation VF, ventricular fibrillation. 

---