Defibrillation and Cardioversion

Chapter 12


Defibrillation and Cardioversion






Introduction


Defibrillation is an emergency procedure performed to terminate ventricular fibrillation (VF) (Fig. 12-1A). VF is a potentially lethal, but survivable “rhythm” commonly found in victims of sudden cardiac arrest (SCA).1,2 VF can be caused by myocardial infarction, myocardial ischemia, undiagnosed coronary artery disease, and electrical injuries. Medications such as tricyclic antidepressants, digitalis, quinidine, and other proarrhythmics can cause QT-segment prolongation and changes in the refractory period of the cardiac cycle that are capable of precipitating VF. Furthermore, chest trauma, hypothermia, cardiomyopathy, electrolyte disturbances, and various toxidromes can induce conditions favoring the development of VF. Hypoxia is another culprit that frequently precipitates VF in adults and the pediatric population. Congenital malformations of the heart and great vessels have also been associated with an increased incidence of VF in young children. The most effective treatment of VF in its early phase is defibrillation.3 It can also be used to terminate pulseless ventricular tachycardia (VT) (Fig 12-1B). Patients with VF or pulseless VT are unresponsive, pulseless, and apneic. These patients sometimes require appropriate integration of cardiopulmonary resuscitation (CPR) with defibrillation to establish the return of spontaneous circulation (ROSC). Other dysrhythmias may also be encountered in patients with SCA, such as pulseless electrical activity (PEA) and even asystole; however, in this chapter discussion is limited to the treatment of VF and pulseless VT.



Defibrillation entails passing a therapeutic burst of electrical current across the chest wall through the myocardium for the purpose of terminating the chaotic electromechanical activity that is impeding the ventricles from ejecting blood into the circulation (Fig. 12-2). Failure to recognize and terminate VF promptly makes suppression of VF via defibrillation more difficult.4 For every minute that the heart is in VF without treatment, the potential for the initial defibrillation to be successful and for the victim of SCA to survive decreases by 7% to 10%.5 However, the integration of CPR with defibrillation, when appropriate, increases the chance for successful defibrillation and survival from SCA.6



Cardioversion is performed to suppress dysrhythmias that produce a rapid pulse and cause the patient to become unstable; such dysrhythmias include supraventricular tachycardia (SVT), atrial fibrillation (AF), atrial flutter, and unstable monomorphic VT (Fig. 12-3). These patients do have a pulse, albeit weak, but can rapidly decompensate, become hypotensive, experience chest pain, or have a change in mental status that will require rapid intervention (i.e., cardioversion). CPR is obviously not indicated because these patients have a pulse and their peripheral tissues are being perfused. Cardioversion is very similar to defibrillation; however, the shock is administered during the refractory period of the cardiac cycle. This is accomplished by setting the defibrillator to the synchronized mode.



The shock is delivered in similar fashion; however, the defibrillator discharges at a particular point in the cardiac cycle. Failure to set the synchronized defibrillator controls properly can result in the conversion of a perfusing rhythm to a nonperfusing rhythm, thereby leaving the patient pulseless.



Principles of Resuscitation


The clinical approach to cardiac resuscitation is an evolving and dynamic endeavor, and guidelines frequently change or are altered. Recommendation from the American Heart Association (AHA) are considered the most reasonable guidelines for the clinician, but many of the principles and caveats are based on minimal data, can be contradictory, and are subject to change; more importantly, any guideline is best applied by considering a specific clinical scenario. Most recently, cardiac resuscitation has been reviewed and new AHA guidelines were released in 2010.7–10 On the basis of the strength of the evidence available, the AHA developed recommendations to support the interventions that showed the most promise. The new algorithms reflect alterations in the sequence of actions to be performed and stress high-quality CPR with compressions of adequate rate and depth that allow complete chest recoil after compressions, minimize interruptions in chest compressions, and avoid excessive overventilation. These modifications stress the interposition of effective CPR (Fig. 12-4) with defibrillation and have been organized in such a way that the time until the first shock is minimized and time to initiation of effective chest compressions is not unnecessarily delayed.




Anatomy, Physiology, and Pathophysiology


The normal human heart rate (HR) is approximately 80 (±20) beats/min. With each beat the heart ejects a stroke volume (SV) of approximately 70 to 80 mL of blood from each ventricle. Multiplying HR by SV produces a value termed cardiac output (CO) (i.e., HR × SV = CO). The product of CO times total peripheral resistance (TPR) produces the value for mean arterial blood pressure (MABP) (i.e., CO × TPR = MABP). When the HR falls to zero or the heart fails to eject an SV (as in VF), MABP drops precipitously. Subsequently, vital organ perfusion is compromised. Hence, blood flow to the brain, the heart, the lungs, and other peripheral organs ceases. Failure to promptly restore blood flow will lead to significant mortality, morbidity, and SCA. Therefore, any interruption in cardiac contraction must be recognized quickly and corrected promptly. Cardiac contraction occurs as a result of a sequence of electromechanical events occurring in myocytes. The human heart has several unique characteristics that enable it to perform its physiologic role. These myocardial characteristics are automaticity, conductivity, excitability, and contractility. Individual cells have a “variable blend” of these characteristics. Some characteristics are more prominent than others, depending on the anatomic location of the cells in the heart. For example, the “pacemaker cells” have more automaticity, the conduction system has increased conductivity, and ventricular free-wall myocytes have more contractility. The electrical properties of these cells can be assessed by performing regional recordings of the changes in voltage in the tissue with respect to time (i.e., action potentials) (Fig. 12-5). The electrical impulse for myocardial contraction originates spontaneously in the sinoatrial (SA) node and spreads through the atria, which causes it to contract. As the impulse arrives at the atrioventricular (AV) node, it undergoes decremental conduction in which the electrical impulse is slowed down as the atria contract and “preload” the ventricles. Subsequently, the impulse activates the bundle of His and Purkinje fibers, which then causes ventricular contraction via excitation-contraction coupling. The electrical events precede the mechanical events. These events are graphically represented in Figure 12-6, which depicts the change in membrane voltage with respect to time as a result of temporal changes in ion permeability across the myocyte membranes. These sequential changes in ion permeability occur as the membrane potential varies, thereby producing the characteristic cardiac action potential.




As the original impulse from the SA node travels through the atria and into the ventricles, various action potentials are generated regionally. The summation of all these action potentials produces the characteristic electrocardiographic (ECG) tracing PQRST (see Figs. 12-5 and 12-6). The ECG tracing is a graphic representation of the electrical activity that induces the mechanical activity of systole. Systole occurs as a result of excitation-contraction coupling. Calcium ion levels in the cytoplasm increase and trigger the contractile proteins to interact. As the ion channels reset, the myocytes return to the resting membrane potential (intracellular calcium is resequestered), and diastole occurs. The membrane pumps restore the ion concentrations to normal. This cycle keeps occurring about 80 times per minute. Each “cardiac cycle” lasts approximately 300 msec. During each cardiac cycle there are two periods that need to be addressed: the absolute and relative refractory periods (Fig. 12-7). During the absolute refractory period, the myocytes do not respond to excitatory stimuli because the channels are in full operation. During the relative refractory period, the myocytes can be stimulated with a stimulus that is proportionately larger than usual as more and more ion channels reset. These facts have relevance with regard to cardioversion and will be discussed further later in the chapter.




Mechanisms of Cardiac Dysrhythmias


As is evident from the preceding discussion, normal cardiac activity is a compendium of complex, sequential electrochemical, physiologic, and mechanical events. It includes three mechanisms: enhanced automaticity, triggered activity, and reentry. If alterations in the action potential phases or a modification of the refractory periods occurs and another impulse stimulates the myocyte at a time that it is out of synch with the normal depolarization-repolarization process, the coordinated normal excitation-contraction coupling becomes asynchronous. If conditions favor the development of ectopic foci, individual loci in the ventricular free walls and septum become “pacemakers” and the myocardium begins to contract uncontrollably (see Fig. 12-2) and produce an irregular ECG tracing (see Fig. 12-1A). CO falls to zero, with SCA ensuing. Another proposed mechanism that can precipitate the development of a dysrhythmia is a malfunction in propagation secondary to errors in conductivity and excitability and reentry of already propagated impulses (Fig. 12-8).





Cardiopulmonary Resuscitation: Ventricular Fibrillation and Pulseless Ventricular Tachycardia


When SCA occurs and the heart is in VF or pulseless VT, ventricular contraction is absent and circulation of blood comes to a standstill. To initiate CPR, mechanically compress the heart between the sternum and vertebral column. This causes pulsatile ejection of blood into the circulation, including the coronary circulation. For these compressions to be effective, perform them quickly and with sufficient displacement of the sternum (i.e., at least 2 inches) to produce adequate flow. Furthermore, keep interruptions in CPR to a minimum so that adequate perfusion pressure is maintained in the vasculature. Although the flow is not at physiologic levels, enough circulation occurs in the tissues, especially the myocardium, that the by-products of VF are “washed out” and the myocardium becomes less refractory to defibrillation.11 During VF, the myocytes are actually consuming oxygen and adenosine triphosphate at a rate believed to be the same or higher than during normal contraction.12,13 Several other concerns must be reinforced. During chest compressions, make sure that the chest recoils completely to the resting state so that blood can enter from the vena cava and pass into the right atrium. The rate of compressions should exceed 100 compressions/min so that adequate forward flow of blood is produced. Remember that HR × SV = CO.



Indications for and Contraindications to Defibrillation


Prompt electrical defibrillation is the most effective treatment of acute SCA and VF.3,4 Prompt initiation of CPR in patients with SCA or VF is also critical for successful resuscitation and ROSC. Starting with the onset of collapse, the survival rate for patients with SCA or VF drops 7% to 10% for every minute of downtime without defibrillation.5 If CPR is initiated, the survival rate declines less rapidly (i.e., 3% to 4% per minute of downtime).4 If an SCA is witnessed and immediate CPR is provided, coupled with immediate defibrillation, survival from such events has been reported to increase up to fourfold.46 Therefore, immediate defibrillation is indicated as soon as VF or pulseless VT is diagnosed. Few absolute specific contraindications to early defibrillation exist other than the presence of a pulse, absence of SCA, medical futility for the procedure, or a valid do-not-resuscitate order.


If a patient is found unresponsive, pulseless, and apneic and the “downtime” is unknown, immediately perform good-quality, effective CPR while preparing for defibrillation. Previous recommendations called for immediate defibrillation in lieu of a short period of CPR. The newest development in the 2010 AHA guidelines for CPR is also a change in the basic life support sequence of steps from the “ABCs” (airway, breathing, chest compressions) to “CAB” (chest compressions, airway, breathing) for adults and pediatric patients (children and infants, excluding newborns). As CPR is performed, prepare for rhythm analysis and initiate defibrillation if indicated. After performing CPR for 2 minutes (5 cycles at a rate of 30 compressions to 2 ventilations), perform rhythm analysis. If VF or pulseless VT is diagnosed, promptly perform defibrillation. When the time until the first shock is delayed during prehospital resuscitation (because of prolonged response times), data have demonstrated that the rate of successful defibrillation increases if patients receive bystander CPR before defibrillation.2–6 A scientific evaluation of this information proposed that CPR enhances the defibrillation threshold by restoring substrates to myocytes for the facilitation or resumption of normal excitation-contraction coupling. Furthermore, CPR may wash out myocardial depressants that have built up during prolonged VF. Therefore, administration of CPR before defibrillation in patients with suspected, prolonged VF is recommended in the prehospital setting. Data to substantiate this sequence for in-hospital resuscitation have not been presented. Thus, the issue of unknown downtime, though not a definitive contraindication to immediate defibrillation, may be a factor in the clinician’s decision-making process regarding the resuscitation sequence.


Victims of SCA as a result of traumatic injuries do not usually survive.13 The heart, aorta, and pulmonary arteries may have sustained injury that will prevent resumption of normal cardiovascular function. There is a high probability that the underlying hypovolemia and organ damage may preclude successful resuscitation. However, the cause of the trauma may have been SCA with subsequent loss of consciousness. In such cases, if SCA or VF is present in a trauma patient, attempt treatment with CPR and defibrillation; if unsuccessful, search for and treat the underlying cause of the trauma and pursue the SCA. Therefore, trauma is not a contraindication to defibrillation, although the resuscitative effort may be futile.


If the victim of VF or pulseless VT is a pregnant female, treatment of the mother is critical. Therefore, prompt defibrillation is indicated as per the same guidelines and sequencing as for nonpregnant patients.14 No harm to the fetus has been reported as a result of defibrillation, and thus pregnancy is not a contraindication to defibrillation.


Previous recommendations suggested delivering a “stacked” sequence of up to three shocks without interposed chest compressions if the first shock was unsuccessful in terminating VF. This was done to decrease transthoracic impedance with the monophasic damped sinusoidal (MDS) defibrillators in use and to deliver more current to the myocardium. However, this recommendation has been rescinded because of lack of supporting evidence. Now, with the higher first-shock efficacy (90%) in successfully terminating VF (termination of VF for 5 seconds) through the use of biphasic defibrillators,8 the recommendation to repeat a shock if the first treatment was unsuccessful is harder to justify. Hence, the AHA now recommends a one-shock protocol for VF. Evidence has accumulated that even short interruptions in CPR are harmful. Thus, rescuers should minimize the interval between stopping compressions and delivering shocks and should resume CPR immediately after delivery of a shock.


Defibrillation is also an effective treatment modality for terminating pulseless VT. If the patient has a pulse, is stable, and has a perfusing rhythm while in VT, defibrillation is contraindicated. However, if the patient in VT becomes unstable and signs of poor perfusion, a change in mental status, or persistent chest pain with pulmonary edema, hypotension, and subsequent shock develop, synchronized cardioversion is recommended. This procedure is addressed later. If the patient becomes unstable as a result of polymorphic VT or becomes pulseless during the episode of VT, an unsynchronized shock (i.e., defibrillation) is indicated.


Patients “found down” or who have just become unresponsive can have other “rhythms present” beside VF or pulseless VT (e.g., PEA or asystole). Defibrillation is contraindicated in individuals with PEA. True asystole is not a shockable rhythm, and current evidence suggests that defibrillating patients with “occult” or false asystole is not beneficial and may actually be harmful. Therefore, defibrillation is contraindicated in patients in asystole as long as fine VF has been ruled out (discussion below).


Some patients who succumb to SCA may have various medication-releasing patches (e.g., nitroglycerin, contraceptive hormones, antihypertensive agents, smoking cessation adjuncts) present on their chest. Their presence is not a contraindication to defibrillation. However, modify the placement of the electrodes or paddles used for defibrillation to avoid contact with these patches. If necessary, remove these items before defibrillation to avoid diversion of current from the myocardium, current arcing, sparks, and other problems.


Developments in defibrillation and computer electronics have led to the availability and use of implantable defibrillators (automatic implantable cardiac defibrillators [AICDs], pacemakers) in the chest of patients who have known coronary artery disease. These patients are prone to dysrhythmias and may have episodes of VT and VF that are automatically detected and defibrillated or cardioverted. However, these devices can malfunction, so if these patients have SCA or VF, perform defibrillation as indicated. The presence of an AICD or pacemaker is not a contraindication to defibrillation. The only caveat is to avoid placement of the defibrillation paddles over the AICD or pacemaker because the current for defibrillation may be redirected away from the fibrillating myocardium and compromise termination of VF. In addition, because current from the defibrillation could enter the AICD or pacemaker, the device could be prone to future malfunction. These devices should be reevaluated after the patient has been defibrillated.


Current trends in fashion sometimes include piercing of the body in various locations. In addition, certain items of clothing and jewelry may require modification of electrode or paddle placement. The presence of metal in locations proximal to the heart or in locations on the chest should be avoided to minimize the potential for diverting the defibrillating current from the myocardium. Also, if the metal object provides a potential short circuit from the patient or leads to “ground,” this object should be removed, if feasible, to avoid diversion of current from the myocardium or arcing and burns across the chest. However, the presence of these materials, such as jewelry or body piercings, is not a contraindication to defibrillation.


In this part of the chapter on defibrillation the recommendations are intended for application to an adult (defined as older than 8 years or weighing more than 25 kg [55 lb]) patient with SCA or VF. If the patient is a child (e.g., 1 to 8 years of age or weighing less than 25 kg [55 lb]), modifications in the sequence, defibrillation energy, energy attenuation equipment, and size of the defibrillation paddles are necessary. Pediatric defibrillation details are discussed later in this chapter. If a defibrillator or automatic external defibrillator (AED) and equipment suitable for use in children are not available, the health care provider can resort to using a standard AED or defibrillator. Use of AEDs or defibrillators in infants younger than 1 year has not been studied.


Defibrillation can be an ignition source for explosion if arcing occurs or if there are any stray or aberrant electrical discharges that occur as a result of paddle or electrode discharge. Therefore, in an environment in which volatile explosive material is present, such as the operating room or other areas of critical care, be careful during defibrillation to avoid electrical arcing and to ensure that electrical conductivity through the patient’s chest is optimal. Avoid using anesthetic agents and oxygen. A potentially explosive environment is a relative contraindication to defibrillation.15


When performing defibrillation, take care to avoid excessive moisture on the chest or around the patient. Although it is unlikely that there will be any significant or dangerous current leaks from the patient onto a wet floor, take care to avoid creating an electrical hazard. Try to ensure that the area is not wet; however, a wet surface is not an absolute contraindication to defibrillation. Defibrillation can be performed on ice and wet pavement.


Finally, defibrillation of an “occult” or “false” asystole or a very fine VF not detectable because of paddle or electrode position may be considered but is not recommended.13 Fine VF can occasionally masquerade as ventricular standstill or asystole. This may be a function of perpendicular electrode orientation with respect to the wavefront of depolarization. When evaluating the rhythm of a patient, if there is any doubt or confusion regarding the type of rhythm present, make sure that several leads are checked and rotate the paddles 90 degrees from their original position to ensure that asystole is indeed present before abandoning the possibility of defibrillation. If fine VF is unmasked, consider providing aggressive CPR before defibrillation. Also, place the controls on the ECG monitor on maximal gain to ensure adequate amplification of weak signals.



Conductive Material


Use of conductive material is important to lower the impedance or resistance to flow of current at the electrode–chest wall interface.16–18 Multiple factors affect the range of impedance (e.g., body weight, chest size, chest hair, moisture on the skin surface of the patient, paddle size [diameter], paddle contact pressure, phase of respiration, and type of conductive material used). High impedance or resistance to flow of current can compromise the amount of current actually delivered to the myocardium and lead to a failed first shock. Inappropriate use of conductive material can result in current bridging or a short circuit and arcing of electrical current secondary to streaking of the material across the chest. This can produce sparks and unnecessary burns on the patient’s skin. In addition, arcing of electricity can become a possible explosion hazard, depending on the circumstances. Conductive material needs to be used with the handheld electrodes. Various electrode gels are available on the market and should be kept in the proximity of the defibrillator, on the prearranged cart ready to use (Fig 12-9A).



Self-adhesive pad electrodes now have a resistance-reducing, conductive material incorporated into the adhesive, thus rendering the use of a gel or other conductive material unnecessary. Firmly applying the self-adhesive electrode pads to the skin will usually be sufficient to minimize impedance, allow adequate ECG acquisition, and if indicated, defibrillate (see Fig. 12-9B).



Procedure



Witnessed Sudden Cardiac Arrest (Figs. 12-10 and 12-11)


When confronted with a patient who has just become unresponsive, prepare for immediate defibrillation (Fig. 12-12). As soon as the defibrillator is available and the patient is connected to the monitor, assess the rhythm. In the interim, turn on the defibrillation equipment, place the paddles or electrodes on the chest, begin assessment of the patient, and initiate the steps in CPR by applying the CAB principle.7






Cardiopulmonary Resuscitation


Perform a pulse check (<10 seconds; see Fig. 12-11, step 1). If a pulse is definitely present, provide 1 breath for 1 second every 5 to 6 seconds or 8 to 10 breaths/min. The breaths can be delivered with either a bag-valve-mask (BVM) or some type of barrier device. Observe the patient for visible chest wall rise and fall so that the thorax dose not become overinflated. Hyperinflation of the chest can lead to inadvertent pressurization of the esophagus, which can cause lower esophageal sphincter pressure to be exceeded. This can lead to retrograde flow of gastric contents into the esophagus with the potential for subsequent aspiration of acid and debris into the trachea if the airway is not adequately protected. Overventilation of the thorax can also lead to an increase in intrathoracic pressure and impedance of blood flow to and from the heart, which should be avoided. Reassess the patient’s pulse every 2 minutes.


If no pulse is present, begin a sequence of 30 chest compressions followed by 2 ventilations/breaths (see Fig. 12-11, step 2). Keep your hands on the lower half of the sternum and compress it at least 2 inches (5 cm) at a rate of at least 100 compressions/min. The time allotted for compression should be 50%/50% for compression and relaxation of the chest. Watch for full chest recoil to allow adequate ventricular filling (do not lean on the chest) before the next compression. When the defibrillator or AED arrives, continue the 30 : 2 ratio of compressions to ventilations during CPR, attach the patient to the defibrillator via electrodes, pads, and paddles applied to the patient’s chest, and initiate the rhythm check (see Fig. 12-11, step 3). Every attempt should be made to minimize interruption of compressions.

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Sep 17, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Defibrillation and Cardioversion
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