Medicine - Cardiac Conduction - Case Study Example

Medicine - Cardiac Conduction Introduction The clinical scenario indicates that this patient, a 46-year-old male presented to the Emergency Department with a presenting complaint of palpitations. Given his cardiac history and his familiarity with Dr. W of cardiology, his presentation history was relevant to the fact that his problem was of cardiac origin. His palpitations or awareness of racing heart began suddenly while he was driving at 12:30, which in his words was racing "over 200 beats per minute." To begin with, he experienced some tightness across his chest which radiated to his jaws and neck. On questioning he denied any light-headedness, loss of consciousness, or shortness of breath. His medication history suggested that he was initially placed on amiodarone for his problems; however, it led to significant side effects of hypothyroidism and gastrointestinal upset. These could have implications on his baseline cardiac disease, and hence it was decided that he be weaned off the medicine, and about 3 months back, he was placed on bisoprolol 2.5 mg in case of tachycardia. He continued to drive for another half an hour and at 1300 hours, when he came back home, he took a 2.5 mg tablet of bisoprolol. From his experience of similar attacks, he found that at this time, the heart beats were taking a longer time to normalise, and in fact, they did not normalise at all, although were slowing. He had previous episodes of atrial fibrillation and had been cardioverted for three occasions in the past. He could recognise that this time, he was not feeling like he had an atrial fibrillation. Thus he was brought in an ambulance to the emergency department. His past medical history is significant for having had rheumatic fever at his age of 12 which was complicated by questionable mild aortic valve incompetence. He was diagnosed with atrial fibrillation for which he was cardioverted in three occasions. In the year 1984, he was diagnosed with Wolf-Parkinson-White syndrome. For these reasons, he was subjected to electrophysiological studies of his heart, where he was recommended to have a cardio ablation. In the year 1988, following a failed attempt at mitral valvuloplasty, he underwent a metallic mitral valve replacement. Over and above that he was also diagnosed to have hypothyroidism due to an adverse effect of amiodarone. He is on thyroxine 120 mg once daily and warfarin 8 mg daily as a prophylactic. His family history is positive strongly for stroke. He is a company director for sales; he is a teetotaler and does not smoke cigarettes. On examination, he looks well with vitals as charted, The mechanical heart click is audible on cardiac auscultation. His chest is clear. Abdomen is soft and nontender. ECG appears to have p waves, demonstrated short PR interval and appearance of delta waves. The treatment plan as decided was to have a Cardiology review. He would be placed on a cardiac monitor. Routine blood needs to be done with a chest X-ray. IV access would be established. This approach has been supported by studies and reports. The impression at this point in time was Wolf-Parkinson-White syndrome (WPW) with now slowing tachycardia. The best course of events would be to repeat an electrophysiological study (EPS) followed by a cardio ablation of the accessory pathway. In this assignment, the underlying basic sciences linking his WPW syndrome, EPS, and ablation will be discussed based on the available evidence from literature. Discussion Cardiac Conduction In all striated muscle cells, muscle contraction is triggered by a phenomenon of rapid voltage change. This is called an action potential. Action potentials occur on the cell membrane. However, action potentials on cardiac muscle cells differ considerably from those arising from the skeletal muscle cells. These differences are important since cardiac contraction has autonomous rhythmic excitation demanded by the physiology, and in normal circumstances this is involuntary. There are three important pathways that promote such synchronous rhythmic excitation of the heart muscles as opposed to the skeletal muscles. These can be self-generating; these are and can be conducted from cell to cell in a direct fashion without any need for higher control; and they may have considerable long durations precluding fusion of these individual contractions which may better be termed as twitches (Spach et al., 1978). Conduction velocity has been defined to be the speed of propagation of the action potential through any region of the cardiac tissue. Since different areas of the heart differ in tissue contents, the conduction velocity would demonstrate considerable variations in different areas of the cardiac musculature and its bulk. This velocity is directly proportional to the diameter of the involved muscle fiber. AV (atrioventricular) node contains for example small-diameter cells. Therefore, conduction through the small-diameter cells in the AV node would be significantly slower than conduction over Purkinje system which consists of large-diameter cells in the same ventricle. There are other determinants of the conduction velocity, which is also directly dependent on the depolarizing currents arising locally and their intensities. Locally arising depolarizing currents are again directly determined by the rate at which the action potential rises. Rapid depolarization dictates rapid conduction. The other determinants of conduction velocities are variations in the capacitive and/or resistive properties of the cell membranes, gap junctions, and cytoplasm, although these differences will be different in specific areas of the heart. The action potentials are initiated by SA node. These then spread progressively across the wall of the atria. It has been observed that action potentials which originate near the SA node and at a point which is distant from SA node would cause similar tracings in the electrocardiogram (ECG) since they have similarly shaped action potentials, although they would be temporally displaced (Wellens 1971). This points to the fact that impulse spread across the atria is a function of time. As indicated earlier, the action potentials that pass through the AV node is inherently slowed down due to the small size of the cell of the AV node leading to a slow rate of rise of action potentials through this. Therefore, the AV node is designed to delay the transmission of the cardiac excitation from the atria to the ventricles. This is physiologically important since this creates a provision of time that is needed for the atrial contraction to contribute to the ventricular filling just prior to the ventricular contraction. It has also been suggested that the cells in the AV node can have a faster spontaneous depolarization throughout the duration of the resting period in comparison to other cardiac cells, the only exception being the cells of the SA node. For this reason, the AV node is sometimes referred to as a latent pacemaker, and in many pathological situations, the AV node takes the upper hand and controls the heart rhythm (Sethi et al., 2007). Electrocardiography Basics The major features of the electrocardiogram are the P, QRS, and T waves. These are caused respectively by the process of atrial depolarization, ventricular depolarization, and ventricular repolarization. P-R interval is the period of time from the beginning of the P wave to the initiation of QRS complex. This indicates the time taken for the action potential to spread across the atria and subsequently to the atrioventricular (AV) node. It should be noted that during the latter portion of the P-R interval, which is known otherwise as PR segment, the electrocardiogram can detect no voltages on the surface of the body. This has been ascribed to the depolarization of the atrial muscle cells. Moreover at this time, the ventricular cells are still in the resting phase. The electrical field set up by those action potentials at this point in time although progressing through the small AV node is not strong enough to be detected by the machine. To assess whether a P-R interval is short, long, or normal, it is important to know the duration of the normal P-R interval. This ranges from 120 to 200 ms. The impulse generated in the SA node is destined to reach AV node and the innate refractory period of it slows down the impulse a bit. Shortly after this cardiac impulse is released out of the AV node, it is transmitted to the Purkinje system which has a rapid conduction velocity (Takagi et al., 1978). Thus, all the ventricular muscle cells can be depolarized within a very short while leading to generation of QRS complex. In any electrocardiogram tracing, the R wave is very prominent. This reflects the depolarization of the ventricular muscle mass. This is large due to the largest and bulkiest ventricular muscle cells which all depolarize almost simultaneously. Normally, the QRS complex duration is between 60 to 100 ms. Thus it is evident that the physiological functions of the specialized conduction systems of the heart are reflected in the electrocardiographic pattern of a normal heart. For example, the transmission of impulse through the AV node and the time taken for it determines the duration of P-R interval. The short duration and large amplitude of the QRS complex reflects the effectiveness of the Purkinje system in synchronizing the process of ventricular depolarization. It should also be noted that nearly every heart muscle cell is inherently capable of rhythmicity (Sternick et al, 2003). This is further facilitated by the fact that all cardiac neuromuscular cells are electrically interconnected through gap junctions, which foster rapid spread of the electrical events of impulse transmission all around. This explains the fact that a functional rhythm in the heart can and often may occur without even involving of part or all of this specialized conduction system when a relevant pathological process may be underlying. Such a situation is, however, abnormal, and the existence of abnormal conduction pathways would produce an abnormal electrocardiogram (Gollob et al., 2000) The WPW syndrome is known as preexcitation syndrome which results in ventricular preexcitation associated with AV bypass tracts. These aberrant connections are composed of strands of muscles which resemble those in the atria, which are very excitable. They are disposed around the AV rings. Although they normally exist, they are not known to be activated always. Most frequently, however, if they are involved in a preexcitation phenomenon evident in the ECG and lead to paroxysmal tachycardias, it is termed as WPW syndrome. Although this patient was not known to have a congenital anomaly of sorts, the most probable reason that he might be having this syndrome is a result of his prior aortic valve surgery which might have implicated one of these aberrant tracts (Sternick et al., 2005). Since the description of WPW syndrome, there had been attempts to explain this electrocardiographic syndrome physiologically. The classic picture consists of a short P-R interval followed by a prolonged QRS complex, where the upstroke is slurred. Obviously, this results from existence of one or more muscular connections between the atria and the ventricles which allow early and aberrant excitation, termed as preexcitation (Hluchy et al., 2000). Research indicated that there indeed are anomalous connections that can be demonstrated histologically. Further research indicated that these actually may be functional atrioventricular bridges. In the WPW syndrome, these AV bypass tracts conduct in an antegrade direction. This produces the typical ECG picture described above. The short P-R interval is less than 0.12 s. The slurred upstroke of the QRS complex is termed as delta wave. Furthermore, the QRS complex is widened. The component systems that contribute to this pattern is a fusion of activation of the ventricles over both the bypass tracts and the AV nodal His-Purkinje system, and the relative contribution of activation over each system dictate the amount of preexcitation (Gmeiner et al., 1984). The abnormally short P-R interval has distinct adverse physiological effects on the patient. In a patient with WPW syndrome, there is a lack of long refractory period of the AV node is lacking. In this case, the patient was known to have atrial fibrillation. In such cases of atrial arrhythmia as in this patient, the occurrence of WPW syndrome would cause a tendency for the ventricles to follow it, which may result in a too fast ventricular rate. A rapid ventricular rate due to bypass of the AV node would lead to inefficient ventricular filling with disastrous consequences for the patient (Lüderitz, 2009). In many cases, the impulses can pass across the AV node and then back along the accessory pathway to restimulate the atria. It is for this reason these patients must be monitored since these accessory pathways of conduction may be the portals for reentry phenomenon which may lead to a potentially life-threatening condition called atrial tachycardia where the short reentry path causes the heart to beat at a very fast rate. It is of utmost importance to prevent atrial tachycardia in a patient with a past history of atrial fibrillation, and atrial tachycardia is very common in patients with WPW syndrome (McHenry et al., 1996). Therefore, serious consideration of treating this syndrome with surgical ablation of the accessory pathway must be given. This patient had atrial fibrillation previously, which is characterised by a complete loss of the normal synchronisation between excitation and refractory periods between the individual atrial cells (Guiraudon et al., 1988), although at this presentation, he did not have any. Furthermore both hypothyroidism and drug induced hyperthyroidism caused by his thyroxine may precipitate hyperexcitability of his atrial muscles. All of these alone or in combination may cause the atria to deploraise, repolarise, and reexcited in a random fashion again and again (Delise et al., 1987). Atrial fibrillation is known to be a self-sustaining process where the excitation impulses are known to enter the AV node at unpredictable times. This situation may be aggravated further by the aberrant pathways responsible for the WPW syndrome. Atrial contractions usually play very minor role in ventricular filling, and therefore, atrial fibrillation is well tolerated by many patients since the ventricular rate can sufficiently maintain ventricular filling and cardiac output (Becker et al., 1978). The problem that may arise from atrial fibrillation is tendency of inordinate coagulation of blood within atria due to absence of atrial contraction which normally are vigorous and coordinated. The patient had been placed on warfarin to counteract this tendency and also to prevent complications from fragmented clots which may be propelled out of the heart to clog the small arterial circulation within other systems of the body. This justifies the anticoagulant therapy in this patient where emboli may compromise critical organ functions (Duszanska et al., 2007). It has been found that during the paroxysmal ventricular tachycardia in a WPW syndrome, the impulse is conducted in an antegrade fashion over the normal AV system of conduction and then a reentry phenomenon occurs where retrograde impulse transmission happens through the bypass tracts (Anderson et al., 1976). In some cases, although rarely, the reverse phenomenon may take place, which may lead to activation of the ventricles by the impulse transmitted through the bypass tracts entirely, leading to a wide QRS complex, which not the case in this patient. It has also been reported that atrial fibrillation is a common occurrence in patients with WPW syndrome (Cotoi et al., 1984). However, this patient needed admission for monitoring since this patient is exposed to the risk of ventricular fibrillation due to the fact that bypass tracts lack the decremental conduction parameters as AV node. This may cause ventricular fibrillation during an episode of superimposed atrial fibrillation on the WPW syndrome that the patient is currently having (Klein et al., 1988). Research has recommended electrophysiological evaluation in such patients despite a positive role of drug therapy as a temporary solution. The alterations in the electrophysiological properties of heart must be investigated by an electrophysiological evaluation of the patient. This is necessary to confirm the diagnosis. The electrophysiological studies would also be able to localise the bypass tracts and would also be enumerate their numbers. During an electrophysiological evaluation, it can be definitely discerned whether a particular aberrant tract is contributing to the evolution of arrhythmia in WPW syndrome (Satake et al., 1996). In fact according to current research, electrophysiological evaluation of the electrical activity of the heart is mandatory in a total assessment and treatment planning of such patients since it not only helps determine the possibility of emergence of life-threatening heart rates during an episode of atrial fibrillation superimposed on WPW syndrome and opens the options for possible definitive therapy (Tsunakawa et al., 1990). Evidence suggests that asymptomatic patients with this preexcitation syndrome do not need any empirical therapy. As in this case, ongoing drug therapy is advised usually for older patients who are symptomatic, specifically when symptoms are infrequent. Despite all these options, the patients who have medically refractory arrhythmia are often offered surgical or nonsurgical ablation of the detected accessory pathway due mainly to the risk of sudden death. Currently, radiofrequency ablation has been established to be a safe, efficient, and definitive management strategy when performed by skilled interventionalists. The patient's clinical and electrocardiographic findings were consistent with WPW syndrome as indicated by the characteristic ECG and other unremarkable findings. The possibility of associated atrial fibrillation had been ruled out. A diagnostic electrophysiological study four multiple electrodes are placed inside the cardiac chambers, and programmed stimulation of these electrodes usually identifies the culprit accessory tract (Lai, 2009). Hemingway et al. (2008) detail the emergency department care of such patients where monitoring is an important part. This patient was not hypoxic, although pulse oximetry is mandatory. The care must be provided in a setting where a defibrillator is mandatory since there is a high possibility that such patients may present with associated atrial fibrillation. This patient had no evidence of cardiac arrest. The presence or absence of atrial fibrillation changes the management considerably. Associated supraventricular tachycardia in WPW syndrome when treated with defibrillation may quite easily precipitate ventricular fibrillation. Atrial fibrillation is an irregular rhythm with evident tachycardia. The treatment goal is to slow the refractory period of AV node so the ventricular rate comes down. If this patient would have associated atrial fibrillation, the principles of treatment would be to prolong the refractory period for the antegrade impulse through the accessory pathway responsible for the WPW syndrome. The slower rate of impulse transmission would eventually slow the ventricular rate since AV nodal impulse will also be low. Since the patient was improving with beta-blockers, it would be rather worthwhile to observe the patient and base him on medical management while planning and preparing for the definitive therapy, although predictability of medical treatment is less and never recommended in unstable patients. This patient has a prior history of atrial fibrillation for which cardioversion was done in three occasions. Quite rightly, he was treated earlier with defibrillator therapy, since drug treatment of atrial fibrillation in case of possible coexistence of WPW syndrome may prove to be disastrous. All these drugs are known to prolong the refractory period of AV node, which might increase the impulse transmission through the responsible accessory pathway leading to ventricular fibrillation in all probability. This patient clinically appeared to have no associated atrial fibrillation in this presentation since he was not very tachycardic and did not feel hypotensive which would indicate hypoperfusion, and therefore, there was no evident instability, hence primary synchronized cardioversion would be unnecessary. It is also to be remembered that these patients must be monitored carefully watching for development of atrial fibrillation or ventricular fibrillation that would be indicated by deterioration or failure to improve. With the earliest sign of these, these patients, however, should be promptly cardioverted (Hemingway et al., 2008). Although pharmacologic therapies have been directed to alter the electrophysiological properties of the heart in WPW syndrome, there is no satisfactory permanent solution possible through pharmacotherapy. All drug therapies essentially increase the refractoriness or decreases the abnormally high conduction velocities through impulse transmission channels. The bypass tracts that transmit abnormal impulses are concealed and the reentrant circuit continues to operate. The agent of choice is usually a beta-blocker such as bisoprolol that would slow conduction and increase the refractoriness of the AV node (Strasberg et al., 1985). If there is a rapid ventricular response, a DC cardioversion is attempted; however, since the patient has a slowing tachycardia at the presentation there may be more time available in order to plan a definitive therapy. Current research recommends surgical ablations of these bypass tracts as a means for permanent cure. However, currently radiofrequency catheter ablation is a better alternative compared to surgery. This option has virtually eliminated the need for surgery virtually. It is to be remembered that radiofrequency catheter ablation of the bypass tracts is not successful in all the cases, although this is the therapy of choice in more than 90% of patients. Studies have shown that it is safer and cost effective, and can offer cure rates that can be comparable to surgery. Despite that in some cases, surgery may be needed (Spencer and Logue, 1974). Following identification of the pathway, a large-tipped catheter is connected to the radiofrequency lesion generator system, designed to deliver radiofrequency at the earliest activation site on the ventricle when the patient remains in sinus rhythm. In the usual practice 20 to 50 w of power is applied seven times for a duration of 10 to 20 seconds successfully ablates the bypass tract which can be documented by reversal of ECG to normal pattern without evidence of characteristic prolonged PR interval, wide QRS complexes and delta waves which may even be evidently maintained at a 4-month followup (Lai, 2009). Conclusion In conclusion, this patient’s WPW syndrome must be treated definitively. To that end electrophysiological studies and ablative therapy must be considered seriously. Research has shown that radiofrequency catheter ablation is the effective alternative in patients who fail medical therapy and who present considerable risks of ventricular fibrillation. If not directly, there can be life-threatening embolic events that may compromise the patient’s clinical situation. This procedure is safe and less costly than surgical ablation. To facilitate this management, a prior localisation of the accessory reentrant pathways for impulse transmission is necessary. Although invasive electrophysiological methods are better and more definitive, there are alternative invasive methods that can localise ventricular preexcitation through standard electrocardiogram, vector cardiogram, and precordial map. It has been reported that used together, these methods may offer a more precise localisation of aberrant pathways in patients with WPW syndrome and hence facilitate successful definite treatment. Although surgical approach has been described in literature as a more definite ablative therapy for patients with proarrhythmic potential, while this patient qualifies for such an approach due to his apparent failure of drug therapy, is not recommended for certain risks. In open surgical approach, highly successful ablation of the accessory pathway can be accomplished either through endo or epicardial dissection of the pathway through the AV groove followed by cryoablation. However given its complications which may be potentially life-threatening, a safer approach may be indicated. It is also to be considered that the disadvantage of open thoracotomy, relatively high mortality, and requirement of prolonged hospital stay all go against the choice. DC catheter ablation has also been abandoned die to serious and unacceptable complications despite its high efficacy rates in ablating the accessory pathway. Radiofrequency energy, on the contrary can cause acceleration of cellular ions and resistive heating of the tissue leading to coagulation necrosis of the accessory pathway with small accurate lesions with discrete borders. This is now the procedure of choice due to fewer occurrences of arrhythmia, complications, no necessity of general anesthesia, and less hospitalization time. It is a high frequency wave and hence it does not stimulate neuromuscular fibers and the success rates of this procedure may range up to 99% depending on the location of the pathway despite the report of mild chest pain during application of RF wave. Although essentially safe certain complications have been reported which include "AV block, pericarditis, cardiac tamponade, acute myocardial infarction, cerebral embolism, air embolism, wall perforation, arteriovenous fistula at groin puncture site, and arterial thrombosis." (Lai, 2009) Reference Anderson RH and Becker AE. (1976). 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