Associate Professor, Liberty University College of Osteopathic Medicine (LUCOM)
Sometimes repolarization to the high level of membrane potential may not occur skin care zits buy flexresan once a day, and membrane potential can remain at the plateau level or at a level intermediate between the plateau level and the resting potential skin care procter and gamble flexresan 5 mg online. The sustained rhythmic activity then can continue at the reduced level of membrane potential and assumes the characteristics of abnormal automaticity skin care news buy 5 mg flexresan amex. However acne 4 months postpartum discount 5 mg flexresan fast delivery, in contrast to automatic rhythms, without the initiating action potential, there can be no triggered action potentials. The ability of the triggered action potentials to propagate is related to the level of membrane potential at which the triggered action potential occurs. The more negative the membrane potential is, the more Na+ channels are available for activation, the greater the influx of Na+ into the cell during phase 0, and the higher the conduction velocity. Therefore, those triggered action potentials have slow upstrokes and are less able to propagate. Consequently, small changes in repolarizing or depolarizing currents can have profound effects on the action potential duration and profile. Such a shift can arise from blockage of the outward current, carried by Na+ or Ca2+ at that time, or enhancement of the inward current, mostly carried by K+ at that time. However, a relief of inactivation for voltages positive to 0 mV leads to a U-shaped voltage curve for steady-state inactivation. Although the genesis of ventricular arrhythmias in these patients is still unclear, marked transmural dispersion of repolarization can create a vulnerable window for development of reentry. The abnormalities of repolarization in hypertrophy and failure are often magnified by concomitant drug therapy or electrolyte disturbances. The exception is when a long compensatory pause follows a premature ventricular complex. Reentry Basic Principles of Reentry During each normal cardiac cycle, at the completion of normal cardiac excitation, the electrical impulse originating from the sinus node becomes extinct, and the subsequent excitation cycles originate from new pacemaker impulses. Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to reexcite the heart after expiration of the refractory period. In pathological settings, excitation waves can be blocked in circumscribed areas, rotate around these zones of block, and reenter the site of original excitation in repetitive cycles. The wavefront does not extinguish but rather propagates continuously and thus continues to excite the heart because it always encounters excitable tissue. Reentrant tachycardia, also called reentrant excitation, reciprocating tachycardia, circus movement, or reciprocal or echo beats, is a continuous repetitive propagation of the activation wave in a circular path, returning to its site of origin to reactivate that site. Although this distinction has a historical background and is useful for didactic purposes, both the anatomical and functional forms can coexist in a given pathological setting and share many common basic biophysical mechanisms. The original 3 criteria for reentry proposed by Mines still hold true: (1) unidirectional block is necessary for initiation; (2) the wave of excitation should travel in a single direction around the pathway, returning to its point of origin and then restarting along the same path; and (3) the tachycardia should terminate when one limb of the pathway is cut or temporarily blocked. Functional block at the center of a circuit occurs when there is block of impulses in otherwise excitable cardiac muscle. When the reentrant circuit forms, the line of block then is sustained by centripetal activation from the circulating wavefront that, by repeatedly bombarding the central area of block, maintains the state of refractoriness of this region. Additionally, it has now been shown that a functional extension of an anatomical line of block can occur such that it plays a role in creating the necessary or critical substrate for reentry. The excitation wavefront propagating in the substrate must encounter unidirectional block; otherwise, the excitation wavefronts traveling down both limbs of the reentrant circuit will collide and extinguish each other. Therefore, a condition necessary for reentry is the maintenance of excitable tissue ahead of the propagating wavefront. In other words, the tissue initially activated by the excitation wavefront should have sufficient time to recover its excitability by the time the reentrant wavefront returns. Thus, conduction of the circulating wavefront must be sufficiently delayed in an alternate pathway to allow for expiration of the refractory period in the tissue proximal to the site of unidirectional block, and there must always be a gap of excitable tissue (fully or partially excitable) ahead of the circulating wavefront. This is facilitated by a sufficiently long reentrant pathway (which is especially important when conduction is normal along the reentrant path), sufficiently slow conduction in all or part of the alternative pathway (because sufficiently long pathways are usually not present in the heart), sufficient shortening of the refractory period, or a combination of these factors. Thus, it is essentially impossible to achieve sustained fibrillation of ventricles of very small, normal, mammalian hearts and equally difficult to achieve sustained fibrillation of the completely normal atria of humans or smaller mammals. The cardiac tissue that constitutes the substrate for reentrant excitation can be located almost anywhere in the heart. Without this central area of block, the excitation wavefront will not necessarily be conducted around the core of excitable tissue; rather, it could take a shortcut, permitting the circulating excitation wavefront to arrive early at the site where it originated. If it arrives sufficiently early, the tissue at the site of origination will still be refractory, and reentrant excitation will not be possible. However, changes in heart rate or autonomic tone, ischemia, electrolyte or pH abnormalities, or the occurrence of a premature depolarization can be sufficient to initiate reentrant tachycardia. The trigger frequently is required because it elicits or brings to a critical state one or more of the conditions necessary to achieve reentrant excitation. In fact, premature depolarizations frequently initiate these tachyarrhythmias because they can cause slow conduction and unidirectional block. Thus, a premature impulse initiating reentry can arrive at one site in the potential reentrant circuit sufficiently early that it encounters unidirectional block, because that tissue has had insufficient time to recover excitability after excitation by the prior impulse. Furthermore, in the other limb of the potential reentrant circuit, the premature arrival of the excitation wavefront causes slow conduction or results in further slowing of conduction of the excitation wavefront through an area of already slow conduction. The resulting increase in conduction time around this limb of the potential reentrant circuit allows the region of unidirectional block in the tissue in the other limb activated initially by the premature beat to recover excitability. It should be noted that the mechanism causing the premature impulse can be different from the reentrant mechanism causing the tachycardia. Because the length and location of the reentrant pathway are relatively fixed, the characteristics of the reentrant circuit are determined by the characteristics of the anatomical components of that circuit. A reentrant tachycardia is initiated when an excitation wavefront splits into two limbs after going around the anatomical obstacle and travels down one pathway and not the other, thus creating a circus movement.
Check vital capacity if neuromuscular respiratory failure possible General examination to look for cause Bruit The former group also requires monitoring for arrhythmia and other forms of autonomic disturbance skin care questionnaire generic flexresan 40mg with mastercard, which are also seen with spinal cord infarction zone stop acne 40mg flexresan visa. A common pitfall is to fail to distinguish true neurological weakness from its mimics acne 415 flexresan 5mg for sale. Patients with systemic illness acne zits order flexresan 20 mg with mastercard, infections, cachexia and depression may report weakness when objective tests of strength are normal. Conversely, patients with systemic illness, pain, or functional disorders may have apparent weakness on examination without there being any neurological dysfunction. In the latter group the observation of give-way weakness, a positive Hoover sign, or inconsistency between the examination findings and functional performance may provide the diagnosis. You should not place undue weight on one aspect of the clinical assessment, but rather consider all aspects of the history and examination together. In difficult cases, reassessment after stabilization, following analgesia and initial investigations, and at intervals thereafter, may be required to reach the correct diagnosis. Even so, the distribution of sensory loss can sometimes seem baffling and inconsistent with the rest of the diagnostic formulation. Reference to dermatome and peripheral nerve field charts, or the appreciation that the sensory signs and symptoms may be due to some other coexistent pathology. It is sometimes worth considering whether the diagnosis is made clearer when the sensory signs are disregarded. Examination Even with a predominantly (or purely) sensory presentation, it is almost always advisable to leave the sensory examination until last, having already developed a clear hypothesis regarding the expected abnormality. Use unaffected region to check patient appreciates what normal sensation is and understands the response expected. Proceed from abnormal to normal areas, mapping out the borders between areas of abnormal and normal sensation. Check spinothalamic (pain/temperature) and dorsal column (vibration/proprioception/light touch) modalities Look for other signs if proprioceptive loss. Cutaneous areas of distribution of spinal segments and sensory fibres of the peripheral nerves: (a) anterior and (b) posterior views. Visual loss may indicate ocular, intracranial or systemic disease that requires prompt intervention to preserve sight. Giant cell arteritis should be considered in any patient over 50 with new-onset visual symptoms: it can present with transient visual loss in one eye (amaurosis fugax), persistent visual loss due to retinal or optic nerve ischaemia (may rarely affect both eyes) or diplopia. Sudden loss of vision typically (but not exclusively) reflects vascular disease, and gradual loss of vision, a non vascular disorder (Table 19. Bilateral visual loss occurs with systemic disease or focal disorders involving the visual pathway from the optic chiasm back to the occipital cortex. Patients may report loss of vision in only one eye, even though both eyes are affected. With a homonymous hemianopia, the patient may only be aware of the visual loss in the eye with the temporal field defect, despite having a nasal visual field defect in the fellow eye. Sudden painless persistent loss of vision is usually due to ischaemia/infarction or haemorrhage at some point along the visual pathway, but is also a feature of retinal detachment (Table 19. Sudden transient loss of vision has a range of ocular, vascular and neurological causes (Table 19. Characteristic field defects seen with lesions at various sites along the pathway are illustrated. The calcarine cortex in the occipital lobe is the location of the primary visual cortex. The occipital lobes are supplied by the posterior cerebral arteries, terminal branches of the basilar artery. Optic neuritis and giant cell arteritis can cause visual loss, which may or may not be associated with pain in the eye. Painless loss of vision is typical of cataract, retinal disorders and disorders of the visual pathway. Drug history A careful drug history is essential as many drugs can cause transient or persistent visual loss (Table 19. Symptoms suggestive of polymyalgia rheumatica/giant cell arteritis (malaise, lethargy, anorexia, weight loss, night sweats, headache, occipital pain, jaw claudication, scalp tenderness) Past eye history, for example cataract surgery or previous uveitis; refractive state, myopic or hypermetropic Drug history Family history Social history, to include occupation and driving status Examination Perform a general examination, with particular attention to heart, blood pressure, carotid and temporal arteries. Defects respecting the vertical midline represent a neurological lesion such as a stroke or compressive lesions. Central defects are caused primarily by age-related macular degeneration or other macular disease. The patient should wear their glasses or contact lenses with any reading correction, if worn. Cover one eye and ask the patient to focus on the central dot with the uncovered eye, then repeat with the other eye. Distortion will be reported if there is macular pathology (age-related macular degeneration or macular oedema). Colour vision Ask the patient to assess the colour quality of a bright red object.
The rationale behind this setting is to pace from a site close to the lesions and shorten conduction time to the ablation site acne underwear order flexresan with amex, thereby allowing detection of delayed activation inside the circular line acne 40s cheap flexresan 10mg with visa. Several criteria are used to define line continuity: (1) low peakto-peak bipolar potentials (less than 0 skin care hospitals in bangalore purchase flexresan 10mg. Importantly acne homemade mask buy flexresan 10 mg free shipping, the only predictive criterion for a successful ablation seems to be the amount of postablation low-voltage encircled area. Electroanatomical mapping is used for real-time monitoring and to tag the ablation sequence. When residual conduction is demonstrated, detailed mapping is performed to identify and ablate gaps in the linear lesion. In contrast, another prospective randomized study comparing the two strategies showed the opposite results. Persistent conduction across to the posterior wall should prompt meticulous online mapping to identify and ablate gaps in the linear lesions. This finding suggests that the benefits demonstrated in previous reports may represent a general debulking of the atria rather than a specific role of electrical isolation of the posterior wall. Additionally, it can eliminate arrhythmogenic triggers arising from the ligament of Marshall. The potential of this complication underscores the importance of an ablation line across the mitral isthmus. One year after the last procedure, 87% of patients with mitral isthmus ablation and 69% without ablation (p = 0. Importantly, continuous linear lesions are difficult to achieve, even under direct visualization during intraoperative ablation. Gaps within the ablation lines, whether secondary to areas of recovery or areas missed initially, can produce areas of slow conduction and a substrate for macroreentry. Fractionated and continuous electrical activity has been assumed to indicate the presence of wave collision, slow conduction, or pivot points where the wavelets turn around at the end of the arcs of functional blocks. First is the "interval confidence level," which characterizes the repetitiveness of the electrogram peaks within the recorded intracardiac signal. The assumption is that the more repetitions are recorded in a given time duration (2. The algorithm allows the operator to exclude both noise and high-voltage signal from the analysis (default values, 0. Some investigators, using unipolar mapping, defined fragmented potentials as electrograms exhibiting two or more negative deflections within 50 milliseconds. Additionally, the baseline signal noise level is determined, and the peak-to-peak electrogram amplitude detection limit is set just higher than the noise level (typically, 0. If the arrhythmias are not successfully terminated by ablation or ibutilide, external cardioversion is performed. However, the clinical role of targeting the sites with high dominant frequency or monophasic action potentials by ablation is still under investigation. The sites of positive parasympathetic responses to high-frequency stimulation are marked on the electroanatomical map. It is important to limit high-frequency stimulation to only 2 to 5 seconds, to avoid eliciting a sympathetic response that can otherwise mask or attenuate the parasympathetic response. The distal electrode of the mapping-ablation catheter is used to deliver high-frequency stimulation (1200 beats/min [20 Hz], at 12 to 24 V and pulse width 1 to 10 milliseconds) using a Grass stimulator (S88X dual output square pulse stimulator, Grass Instruments Division, Astro Med Inc. Tolerance of the conscious patient to the stimulation still must be determined, because most reports have described use of this approach in deeply sedated patients. Once identified, the location of a ganglionated plexus is tagged on the electroanatomical map. For anatomically guided atrial autonomic denervation, the endpoint of the ablation procedure is elimination of electrical activity (peak-to-peak bipolar electrogram less than 0. P wave onset or a monophasic, narrow, and positive P wave in lead V1 during ectopy. The polarity of the P wave of the ectopic beat in the inferior leads is a useful method to differentiate the location of the ectopic beats. However, the endocardial approach is the best method for differentiating ligament of Marshall ectopy from other sources. One explanation is epicardial activation via the myocardial tissue within the vein of Marshall. Despite this exit delay, however, the earliest atrial activation should be in the perivenous area. Left, Pace mapping replicates the atrial activation sequence during the ectopy complex. Infrequently, endocardial ablation alone cannot eliminate all connecting fibers, as evidenced by the ability to still record ligament of Marshall potentials. Even using an irrigated-tip catheter and a high-power setting, complete isolation still may not be possible. Cannulation of the vein of Marshall can be used to guide epicardial ablation sites. Pacing prior to ablation along the circumference of this vein at an output between 5 and 10 mA is mandatory before energy delivery. The maneuver should be repeated at each ablation site, and during ablation the catheter should not be moved to sites more than a few millimeters away. Some operators have advocated isolation of the appendage as a means of eliminating these arrhythmias without entering the deeper part of the appendage, which typically turns back medially toward the midline (limiting catheter reach) and where muscle is very thin. The appendage is occasionally inadvertently isolated during roof or mitral isthmus line ablation. Alternatively, anatomically based ablation around the ostium or the appendage can be performed, guided by a mapping system, because much of the line will have already been made with prior ablation. A combined endocardial and epicardial approach to ablate ligament of Marshall ectopy has a higher success rate (60% to 70%).
Unipolar recordings are usually of little help when mapping arrhythmias associated with regions of scar acne cyst removal flexresan 40 mg fast delivery, unless the recordings are filtered to remove far-field signal skin care myths buy flexresan 40mg without prescription. Much of the far-field signal in a unipolar recording consists of lower frequencies than the signal generated by local depolarization because the high-frequency content of a signal diminishes more rapidly with distance from the source than the low-frequency content skin care 90036 trusted 30 mg flexresan. Electrical activity spans the tachycardia cycle length (shaded); thus skin care while pregnant discount flexresan 20 mg fast delivery, a merely presystolic electrogram is a poorindicatorofoptimalablationsite. After leaving the exit of the isthmus, the circulating wavefront propagates through a broad path (loop) along the border of the scar, back to the entrance of the isthmus. In such circuits, repositioning of the catheter to other sites may allow visualization of what is termed bridging of diastole; electrical activity in these adjacent sites spans diastole. Such sites can reflect late activation and may not be related to the tachycardia site of origin. Additionally, electrical signals that come and go throughout diastole should not be considered continuous. For continuous activity to be consistent with reentry, it must be demonstrated that such electrical activity is required for initiation and maintenance of the tachycardia, so that termination of the continuous activity, either spontaneously or following stimulation, without affecting the tachycardia, would exclude such continuous activity as requisite for sustaining the tachycardia. Furthermore, the continuous activity should be recorded from a circumscribed area, and motion artifact should be excluded. Mid-Diastolic Activity An isolated mid-diastolic potential is defined as a low-amplitude, high-frequency diastolic potential separated from the preceding and subsequent electrograms by an isoelectric segment. Sometimes, these discrete potentials provide information that defines a diastolic pathway, which is believed to be generated from a narrow isthmus of conduction critical to the reentrant circuit. Therefore, regardless of where in diastole the presystolic electrogram occurs (early, middle, or late), its position and appearance on initiation of the tachycardia, although necessary, does not confirm its relevance to the tachycardia mechanism. One must always confirm that the electrogram is required to maintain, and cannot be dissociated from, the tachycardia. These potentials remain fixed to the prior tachycardia complex (exit site from the isthmus), and a delay between this complex and the subsequent tachycardia complex would reflect delay in entering or propagating through the protected diastolic pathway. Time-consuming, point-by-point maneuvering of the catheter is required to trace the origin of an arrhythmic event and its activation sequence in the neighboring areas. The success of roving point mapping depends on the sequential beat-by-beat stability of the activation sequence being mapped and the ability of the patient to tolerate sustained arrhythmia. Therefore, it can be difficult to perform activation mapping in poorly inducible tachycardias, in hemodynamically unstable tachycardias, and in tachycardias with unstable morphology. Sometimes, poorly tolerated rapid tachycardias can be slowed by antiarrhythmic agents to allow for mapping. Alternatively, mapping can be facilitated by starting and stopping the tachycardia after data acquisition at each site. Although activation mapping is adequate for defining the site of origin of focal tachycardias, it is deficient by itself in defining the critical isthmus of macroreentrant tachycardias, and adjunctive mapping modalities. Moreover, the laborious process of precise mapping with conventional techniques can expose the electrophysiologist, staff, and patient to undesirable levels of radiation from the extended fluoroscopy time. Using conventional activation mapping techniques, it is difficult to conceive the three-dimensional orientation of cardiac structures because a limited number of recording electrodes guided by fluoroscopy is used. The inability to associate the intracardiac electrogram with a specific endocardial site accurately also limits the reliability with which the roving catheter tip can be placed at a site that was previously mapped. This results in limitations when the creation of long linear ablation lesions is required to modify the substrate, as well as when multiple isthmuses or channels are present. The inability to identify, for example, the site of a previous ablation increases the risk of repeated ablation of areas already dealt with and the likelihood that new sites can be missed. Entrainment Mapping Fundamental Concepts To help understand the concept of entrainment, a hypothetical reentrant circuit is shown in Figure 5-14. This reentrant circuit has several components-a common pathway, an exit site, an outer loop, an inner loop, an entry site, and bystander sites. The reentrant wavefront propagates through the common pathway (protected critical isthmus) during electrical diastole. Because this zone is usually composed of a small amount of myocardium and is bordered by anatomical or functional barriers preventing spread of the electrical signal except in the orthodromic direction, propagation of the wavefront in the protected isthmus is electrocardiographically silent. The exit site is the site at which the reentrant wavefront exits the protected isthmus to start activation of the rest of the myocardium, including the outer loop. The outer loop is the path through which the reentrant wavefront propagates while at the same time activating the rest of the myocardium. An inner loop can serve as an integral part of the reentrant circuit or function as a bystander pathway. If conduction through the inner loop is slower than conduction from the exit to 100 entrance sites (through the outer loop), the inner loop will serve as a bystander, and the outer loop will be the dominant. If conduction through the inner loop is faster than conduction through the outer loop, it will form an integral component of the reentrant circuit. Bystander sites are sites that are activated by the 5 reentrant wavefront but are not an essential part of the reentrant circuit. When a premature stimulus is delivered to sites remote from the reentrant circuit, it can interact with the circuit in different ways. When the stimulus is late-coupled, it can reach the circuit after it has just been activated by the reentrant wavefront. Consequently, although the extrastimulus may have resulted in activation of part of the myocardium, it fails to affect the reentrant circuit, and the reentrant wavefront continues to propagate in the critical isthmus and through the exit site to produce the next tachycardia complex on time. If the extrastimulus encounters fully excitable tissue, as commonly occurs in reentrant tachycardias with large excitable gaps, the tachycardia is advanced by the extent that the paced wavefront arrives at the entrance site prematurely. If the tissue is partially excitable, as can occur in reentrant tachycardias with small or partially excitable gaps, or even in circuits with large excitable gaps when the extrastimulus is very premature, the paced wavefront will encounter some conduction delay in the orthodromic direction within the circuit. Consequently, the degree of advancement of the next tachycardia complex depends on both the degree of prematurity of the extrastimulus and the degree of slowing of its conduction within the circuit. Therefore, the reset tachycardia complex may be early, on time, or later than expected.
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