David A. Wald, DO

• Associate Professor
• Department of Emergency Medicine
• Temple University School of Medicine
• Philadelphia, Pennsylvania

The alkalosis persists even after the kidneys have had more than enough time to fully eliminate the excess bicarbonate androgenic hormone baldness . Oxygen Diffusion Capacity In response to short-term exposure to high altitude androgen hormone zone , there are a number of factors that limit oxygen diffusion prostate cancer death rate . At altitudes greater than 2500 meters prostate drainage , even the estimated at-rest pulmonary capillary transit time of 0 man health after 40 . This diffusion limitation is exacerbated during exercise because of the shortened transit time of blood moving through the alveolar-capillary system mens health survival of the fittest cardiff . With long-term residence at high altitude, there is a remarkable change in the oxygen diffusion capacity, although the mechanism remains unclear. High-altitude natives have been shown to have an oxygen diffusion capacity that is about 20 to 25 percent greater than predicted, both during rest and exercise. The increased oxygen diffusion may be explained, in part, by the polycythemia that often develops at high altitudes. The increased oxygen diffusion may also be explained by the larger lung volumes or capacities seen in high-altitude natives. It is suggested that the larger lungs provide an increased alveolar surface area and a larger capillary blood volume. This is further supported by studies that demonstrate that when animals are exposed to low-oxygen partial pressures during their active growth period, they develop larger lungs and greater diffusion capacity. On the other hand, animals exposed to high concentrations of oxygen during their active growth period develop smaller lungs than expected. Thus, as the blood leaves the alveolar-capillary system, there is a large P(A2a)O characteristic of oxygen diffusion limitations. Twenty percent of the PaO did not move across the alveolar-capillary membrane into the capillary blood. At high altitude, the P(A2a)O is further increased (1) during exercise-because of the increased cardiac output-and (2) in individuals with alveolar thickening caused by interstitial lung disease. Cardiac Output During acute exposure to a hypoxic environment, the cardiac output during both rest and exercise increases, which in turn increases the oxygen delivery to the peripheral cells. In individuals who have acclimatized to high altitude, however, and in high altitude natives, increased cardiac output is not seen. The precise reason for the return of the cardiac output and oxygen uptake to sea level values is unknown. It has been suggested that the polycythemia that develops in well-acclimatized subjects may play a role. As the blood leaves the alveolar-capillary system, there is a large alveolar-arterial oxygen tension difference P(A2a)O. It is known, however, that it is the partial pressure of oxygen in the alveoli, not the partial pressure of arterial oxygen, that chiefly controls this response. Other Physiologic Changes Sleep Disorders During the first few days at high altitude, lowlanders frequently awaken during the night and complain that they do not feel refreshed when they awake in the morning. When sleeping, they commonly demonstrate breathing that waxes and wanes with apneic periods of 10- to 15-second duration (Cheyne-Stokes respiration). One such innovation is the use of hypobaric, or high altitude, chambers for sleep. Regulated airflow in and out of the chamber is maintained to allow for fresh oxygen and the evacuation of carbon dioxide. At increased altitudes-those greater than sea level-the barometric pressure is reduced in proportion to the increase in altitude. Although oxygen is still present at 21 percent-room air equivalent-the decrease in overall barometric pressure means an overall decrease in the partial pressure of inspired oxygen. Hypobaric chambers can simulate altitudes of up to 14,500 feet, which is a barometric pressure equivalent of about 451 mm Hg. This means the partial pressure of atmospheric oxygen in the sleep chamber is only about 95 mm Hg. The higher the altitude that is being mimicked, the lower the inspired oxygen and, consequently, the more hypoxemia that is experienced. The general rationale for this type of training is this: Hypoxemia is a stimulus for the increased production of erythropoietin, which in turn stimulates the production of more red blood cells. Theoretically, by increasing the red blood cell production, the athlete can increase oxygen delivery to working muscles during competition-which in turn should enhance overall athletic performance. The hypobaric chamber offers a means to obtain the benefits of altitude training, without the travel and other inconveniences. Thus, the athletes can "live high" during sleep and "train low" while working out at atmospheric pressures in their own environments. Myoglobin Concentration the concentration of myoglobin in skeletal muscles is increased in high-altitude natives, and studies of this group have shown a high concentration of myoglobin in the diaphragm, the adductor muscles of the leg, the pectoral muscles, and the myocardium. Symptoms usually do not occur until 6 to 12 hours after an individual ascends to a high altitude. It is suggested that the primary cause is hypoxia, complicated by the hypocapnia and respiratory alkalosis associated with high altitude. It may also be linked to a fluid imbalance because pulmonary edema, cerebral edema, and peripheral edema are commonly associated with acute and chronic mountain sickness. In some cases, descent to a lower altitude may be the only way to reduce the symptoms. High-Altitude Pulmonary Edema High-altitude pulmonary edema is sometimes seen in individuals with acute mountain sickness. A typical scenario is as follows: A lowlander rapidly ascends to a high altitude and is very active during the trip or chapter 19 High Altitude and Its Effects on the Cardiopulmonary System 573 upon arrival. Initially, the lowlander demonstrates shortness of breath, fatigue, and a dry cough. It may be associated with the pulmonary vasoconstriction that occurs in response to the alveolar hypoxia. It may also be associated with an increased permeability of the pulmonary capillaries. High-Altitude Cerebral Edema High-altitude cerebral edema is a serious complication of acute mountain sickness. It is characterized by photophobia, ataxia, hallucinations, clouding of consciousness, coma, and possibly death. It is suggested that it may be linked to the increased cerebral vasodilation and blood flow that result from hypoxia. It is characterized by fatigue, reduced exercise tolerance, headache, dizziness, somnolence, loss of mental acuity, marked polycythemia, and severe hypoxemia. A hematocrit of 83 percent and hemoglobin concentrations as high as 28 g/dL have been reported. As a result of the high hematocrit, the viscosity of the blood is significantly increased. Finally, high altitudes disrupt normal sleep patterns; increase myoglobin in the skeletal muscles; and can cause acute or chronic mountain sickness, pulmonary edema, and cerebral edema. The clinical connection associated with these topics discusses hypobaric sleep and athlete training. The barometric pressure is about half the sealevel value of 760 mm Hg at an altitude of A. When an individual is subjected to a high altitude for a prolonged period of time, which of the following is(are) seen In individuals who have acclimatized to a high altitude, an increased cardiac output is seen. There is a linear relationship between the degree of ascent and the degree of pulmonary vasoconstriction and hypertension. Natives who have been at high altitudes for generations commonly demonstrate a mild respiratory alkalosis. The concentration of myoglobin in skeletal muscles is decreased in high-altitude natives. Introduction High-pressure environments have a profound effect on the cardiopulmonary system. Such environments are encountered in recreational scuba diving, deep sea diving, and hyperbaric medicine. The effects of highpressure environments on the cardiopulmonary system are typically studied in (1) actual dives in the sea; (2) hyperbaric chambers, where the subject is exposed to mixtures of compressed gases (known as "simulated dry dives"); and (3) a water-filled hyperbaric chamber that can simulate any depth by adjusting the gas pressure above the water (known as "simulated wet dives"). Diving Because water is incompressible, the pressure increases linearly with depth. Breath-Hold Diving Breath-hold diving is the simplest and most popular form of diving. Up to 30 minutes of so-called oxygen hyperventilation is allowed under the Guinness guidelines. The reader is challenged to consider the following: Assuming an average total lung capacity, approximately how much oxygen did Mr. Note, however, that hyperventilation prior to a breath-hold dive can be dangerous. Should this happen, the diver could lose consciousness before reaching the surface and drown. In fact, the gas pressure in the lungs is about doubled when the diver reaches a depth of 33 feet (2 atm). The mammalian diving reflex is a set of physiologic reflexes that acts as the first line of defense against hypoxia. The diving reflex may partially explain the survival of numerous near-drowning cases in cold water after submersion lasting more than 40 minutes. It is suggested that the peripheral vasoconstriction elicited during a deep dive conserves oxygen for the heart and central nervous system by shunting blood away from less vital tissues. The amount of dissolved gas that enters the tissues is a function of (1) the solubility of the gas in the tissues, (2) the partial pressure of the gas, and (3) the hydrostatic pressure in the tissue. When the decompression is performed at an appropriately slow rate, the gases leaving the tissues will be transported chapter 20 High-Pressure Environments and Their Effects on the Cardiopulmonary System 581 (in their dissolved state) by the venous blood to the lungs and exhaled. When the decompression is conducted too rapidly, the gases will be released from the tissue as bubbles. Depending on the size, number, and location of the bubbles, they can cause a number of signs and symptoms, collectively referred to as decompression sickness. Decompression sickness includes, but is not limited to , joint pains (the bends), chest pain and coughing (the chokes), paresthesia and paralysis (spinal cord involvement), circulatory failure and, in severe cases, death. Barotrauma While diving, the increased pressure can cause tissue injury in the lungs, middle ear, paranasal sinuses, and gastrointestinal tract. Middle-ear barotrauma is the most common diving-related disorder encountered by divers. Barotrauma can occur in the alveoli distal to a blocked airway, in a paranasal sinus with an obstructed orifice, in a small pocket of air left between a tooth filling and the base of the tooth, or in the air space within a diving mask (mask squeeze). Facial edema, ecchymoses (bluish discoloration of an area of skin), and conjunctival hemorrhages are often observed after diving. Gastrointestinal barotrauma may also occur when air enters the stomach as a result of a faulty breathing apparatus or by swallowing air. In extreme cases, an overextended stomach may rupture and lead to a condition known as pneumoperitoneum (air in the peritoneal cavity of the abdomen). Hyperbaric Medicine the administration of oxygen at increased ambient pressures is now being used routinely to treat a variety of pathologic conditions. Clinically, this therapy is referred to as hyperbaric medicine and is accomplished by means of a hyperbaric chamber. Most of the therapeutic benefits of hyperbaric oxygenation are associated with the increased oxygen delivery to the tissues. Very little additional O2 can be combined with hemoglobin once this saturation level is reached. However, the quantity of dissolved O2 will continue to rise linearly as the PaO increases. The breath-hold diver uses the oropharyngeal musculature to pump boluses of air into the lungs to increase the volume above his or her normal total lung capacity. Although the experienced breath-hold diver can increase their lung volumes by up to 3 L, this maneuver is associated with hypotension, decreased cardiac output, pulmonary barotrauma, and pneumomediastinum. Hyperbaric oxygen has long been useful in the treatment of diseases such as decompression sickness and gas embolism. Regardless of the cause of the bubbles, hyperbaric oxygen is effective in reducing bubble size, accelerating bubble resolution, and maintaining tissue oxygenation. Hyperbaric oxygen is used empirically to enhance wound healing in conditions associated with ischemic hypoxia. Clinically, such conditions include radiation necrosis of bone or soft tissue, diabetic microangiopathy, compromised skin grafts, crush wounds, acute traumatic ischemias, and thermal burns. For these conditions, it appears that hyperbaric oxygen increases both the tissue oxygenation and capillary density. Clinical evidence supports the use of hyperbaric oxygen for the treatment of anaerobic infections, including clostridial myonecrosis (gas gangrene); a variety of necrotizing soft-tissue infections; and chronic refractory osteomyelitis. Hyperbaric oxygen added to surgery and antibiotics in the treatment of clostridial myonecrosis increases tissue salvage and decreases mortality.

Under these conditions androgen hormone in men , the lithium/iodine battery can maintain an adequate voltage even when its internal resistance reaches several thousand ohms prostate joint pain . On the other hand mens health blog , an implantable cardiac defibrillator may have peak power requirements approximately 10 prostate nomogram ,000 times greater than those of a pacemaker prostate cancer 20s . Under such a high power demand the voltage of a lithium/iodine battery would drop to almost zero and the power delivered to the device would be almost nil prostate young living . In recent years the distinction between a need for high- and low-rate batteries has become somewhat more blurred because features like distance ("wireless") telemetry and multisite pacing need both more current and more capacity to operate. The result is that battery designers have been challenged to develop more medium-rate batteries that can deliver more power than pacemaker batteries of the past while still having a high energy density. Average Versus Instantaneous Current Drain Implantable medical devices are often characterized by their average current drain. However, average current drain does not tell the entire story because certain events, such as therapy delivery and telemetry, may require temporary current excursions that can be very different from the average value. Sometimes the effect of the instantaneous current demand can be mitigated by the use of a capacitor that buffers the battery to allow short bursts of power that may be more than two orders of magnitude higher than it could deliver directly. This allows the use of battery designs with reduced anode and cathode surface areas and improved volumetric efficiency. Shape, Size, and Mass Constraints Finally, all device requirements (longevity, end-of-service indication, peak power, and so on) must be balanced against device volume, shape, and mass. Volume and thickness are particularly important for safe implantation in children and for esthetic reasons in many adults. The flashlight that does not work when needed after prolonged storage is a good example. One mechanism by which self-discharge can occur involves a slow direct reaction between the anode and the cathode. This can occur if one or both of the active electrode materials are very slightly soluble in the electrolyte. Other self-discharge processes may involve reactions between either the anode or the cathode and another substance in the battery, such as the solvent in the electrolyte. A typical example of this would be a reaction between the anode and the electrolyte solvent to form a passive film on the lithium anode or to form a gas that pressurizes the battery case. These parasitic reactions are usually very slow, but because medical batteries are expected to operate for many years, their accumulated effects can be appreciable. Some parasitic reactions, such as the reaction between lithium and electrolyte, may not become apparent for a long period of time because implantable batteries are typically designed with an excess of lithium. Although it is hard to measure the very slow rate of self-discharge or other parasitic reactions, techniques such as microcalorimetry, which can detect the small amounts of heat that are involved, have been used for this purpose. Assessment of self-discharge is an important element in the creation of accurate predictive models of battery performance that can be used both in device design and longevity estimation. The most important requirement in battery selection for implantable devices is high reliability. Other significant factors include the desired longevity of the device (directly related to battery energy density, circuit design, and overall device size) and an appropriate indication of impending battery depletion (end-of-service warning). The basic considerations when designing a battery for an implantable medical device include the current variations that can be expected from the circuit as the device provides its service for individual patients. The operating current and longevity demanded of the battery determine both the minimum areas and the amounts of the anode and the cathode needed. Increasing the electrode area-to-volume ratio increases current capability, but this ratio must not be made too large or the battery will be too costly, have a diminished energy density, and most likely have greater complexity (a cause for reliability concerns). Relationship Between Size, Energy Density, and Current Drain the relationship between battery size and average current is not one of direct proportionality. For example, decreasing the average current by 50% will not permit a 50% reduction in battery size without compromising longevity because of the inactive materials in a battery (case, electrolyte, current collectors, and the like). Likewise, the usable energy density is also a function of the current demand on the cell. Thus useable energy density, which is directly proportional to the area under the discharge (voltage vs. The Battery and Longevity of the Pulse Generator Longevity is typically defined as the interval between device implantation and detection of the end-of-service indicator. Because therapy can vary substantially from patient to patient, the longevity requirement is typically linked to a specified set of nominal conditions and programmed parameters. The minimum battery capacity required to achieve the specified longevity can be calculated from the average current needed for this nominal set of conditions. The following equation relates the longevity of the pulse generator, L, to the deliverable capacity of the battery, Qdel, and the average pacing current, I. Effect of Pulse Width on Pacing Current Increasing the pacing rate, pulse width, or pulse amplitude increases the average pacing current. The average pacing current, excluding overhead current, is directly proportional to the pacing rate. Recall that the pacing pulse results from the discharge of a capacitor through the electrode-heart interface. This is because additional capacity is needed to account for selfdischarge and other parasitic losses of capacity (Qsd). The area under each current-time curve gives the total charge delivered during the pulse. Nevertheless, reducing the pulse width by a given fraction will always reduce the average pacing current by a substantially smaller fraction because of the exponentially decaying shape of the pacing stimulus current curve. Effect of Pulse Amplitude on Pacing Current the definition of pacing pulse amplitude may vary somewhat between manufacturers of implantable pulse generators. For our purposes, pulse amplitude is defined as the voltage delivered to the heart at the beginning of the pacing pulse (leading edge voltage). As stated earlier, the area under the current-time curve gives the charge delivered per pulse. Thus doubling the amplitude doubles the current and the total charge delivered to the heart. It might also seem that because the charge per pulse is doubled, the average pacing current drawn from the battery would also be doubled. However, the impact on the pacing current is much larger than that, as seen from the following argument. It has two main components: the static current drain, which powers the electronic components even when no therapy is delivered, and the therapeutic current. The trend throughout the evolution of implantable devices has been that current demands decrease as technology is improved and this leads to smaller batteries and pulse generators while maintaining relatively constant longevity. There is some expectation that this trend will continue, but the path to lower current often has a saw tooth profile as new features and therapeutic modalities temporarily increase the required current. From this equation it is readily apparent that energy consumption increases with the square of the output voltage. The effect of this energy increase on the current drawn from the battery may not be intuitive. Because the battery supplies all of the energy delivered to the heart at a relatively constant voltage, any increase in energy is accompanied by a proportional increase in current drawn from the battery. In fact, this is the best situation; additional energy losses occur when the stimulus voltage is programmed to a higher level because the electronic circuit for increasing the stimulus voltage is not 100% efficient. The current drained from the battery can be markedly increased when the pacing stimulus amplitude is programmed to a value higher than the redox potential of the battery chemistry. For example, if a pulse generator is programmed to deliver stimulus amplitude of 5 V using a lithium iodide battery generating 2. The most common way to do this for pacing circuits is to charge a number of capacitors in parallel and then rearrange them electronically into a series configuration so the voltages are then additive. This is also the way a defibrillator pulse voltage is created, although such circuits also use a flyback transformer to efficiently achieve the very high voltages in a defibrillation discharge. The impedance of the lead, itself, is mainly a resistance and it is relatively small (50-100 ohms). Most of the "lead" impedance actually arises at the electrode-tissue interface (500-1000 ohms or more). In general, the average pacing current is approximately inversely proportional to the sum of the actual lead and tissue interface impedances. Summary of Programming Effects on Longevity of Bradycardia Pulse Generators In summary, the wide range of pacing parameters that can be selected can have a dramatic effect on the current drain from the battery in an implanted pulse generator. For example, in the same patient, a bradycardia pulse generator with 6 years of longevity under nominal pacing parameters may reach its replacement time in 2 years at one extreme or more than 10 years at the other extreme. Although such ability is clearly useful, it also can consume significant battery capacity if done too frequently; thus it becomes one more important factor for consideration in device longevity. In general, the two other largest factors to consider are the expected frequency of tachyarrhythmia therapies and the percentage of time spent pacing the heart. It is possible for the longevity to vary by a factor of two to three due to these issues alone. In general, this requires a battery to have some measurable characteristic, such as voltage or impedance, which can be related to its state of discharge. The pulse generator end-ofservice indication must occur well before the battery loses so much voltage that it cannot sustain cardiac pacing or perform defibrillation. Because longevity is a strong function of device settings, the longevity requirement is typically linked to a specific set of nominal pacing or defibrillation parameters. A detailed knowledge of the variations in battery performance, the changes in load current with pulse generator settings, and the accuracy of the end-of-service measurement circuitry is necessary to ensure that these requirements will be met. Typically, this indicator is designed to occur at least 3 months before the battery voltage drops to a level that would result in erratic pacing, loss of capture, or loss of other critical features. Battery Voltage the most common method to indicate impending battery depletion is to measure the battery voltage. Most modern devices incorporate a voltage measurement circuit in the form of an analog-to-digital converter. For lithium/iodine batteries, the battery voltage remains relatively constant throughout most of its discharge under low load conditions. Notice that the resistance changes from a modest value at the beginning of service to a quite large value when it is nearly depleted. Voltage characteristics during discharge differ for different battery chemistries. Therefore the clinician should not assume a familiarity with one model implantable device or one type of battery can be applied to another device or battery chemistry. However, because the measurement of consumed charge is never 100% accurate, the measurement error tends to accumulate over time, making it difficult to accurately predict remaining battery life as the battery nears depletion. On the other hand, implantable batteries are typically designed to have a declining voltage as they near depletion, making voltage measurement a much more accurate monitor in this region. Some devices now switch from one mode of measurement to another as the battery is depleted. The user is simply presented with information regarding the remaining battery life and is not necessarily informed about the particular methodology used to arrive at that estimate. This is particularly true for the lithium/iodine battery because of its significant impedance. The battery voltage is usually measured during normal sensing and pacing operation and not during a defibrillation therapy when the battery voltage is depressed. This approach is possible because most battery designs have a reduced power capability as the battery approaches depletion. In fact, there are often significant variations between various models provided by a single manufacturer. The first three mainly pertain to older pacemakers that may still be implanted in some patients. Recommended replacement time is indicated by a change in the pacing rate to a predetermined fixed rate (such as 65 bpm) or a fractional change in rate (such as a 10% decrease from the programmed rate). The magnet-pacing rate decreases in a stepwise fashion related to remaining battery life. In modern pacemakers the battery voltage or the battery impedance can be telemetered to the programming device. All manufacturers provide technical manuals containing tables or graphs that indicate the relationship between battery voltage or impedance and the estimated remaining service life of the device. This voltage is much less sensitive to current variances than is the voltage chosen for a lithium/iodine battery because the internal resistance of this battery is much lower than the lithium/iodine battery; so for this system, voltage is a good indicator of remaining service life. Battery Impedance Battery impedance is another parameter used to signal the elective replacement point. At depletion, lithium/iodine battery impedance is not only useful for signaling the elective replacement point but may also provide an estimate of remaining service life. Consumed Charge A final method used to indicate remaining battery life has been to measure the cumulative sum of the charge removed from the battery. This is accomplished by monitoring the current drawn from the battery or the current plus voltage. This method requires an accurate knowledge of the original deliverable capacity of the battery because the technique actually measures the capacity already used, and the amount left must be calculated by subtracting this from the initial value. Blended Methods It is becoming more common to determine remaining battery life by blending two or more of the methods described above. For example, many battery chemistries produce a relatively unchanging voltage and impedance in the early part of their discharge. The first implant of a pacemaker powered by a lithium/ iodine battery occurred in 1972.

Delayed aneurysm rupture after flow diversion is uncommon prostate exam meme , and adjunctive coiling may decrease its incidence by promoting intra-aneurysm thrombosis prostate 5lx . Careful inspection of the flow diverter for its apposition to the parent vessel wall can detect an endoleak mens health 90 second ab blaster , which can result in persistent aneurysm filling and thromboembolic complications androgen hormone function . Recanalization can be detected on routine follow-up imaging or can result in new or recurrent neurological symptoms prostate cancer 9 score . However prostate cancer odds , deconstructive treatment with parent vessel occlusion carries a risk of ischemic stroke even if patients successfully pass balloon test occlusion. Management of antiplatelet therapy in patients undergoing neuroendovascular procedures. Long-term clinical and imaging followup of complex intracranial aneurysms treated by endovascular parent vessel occlusion. Resolution of cranial neuropathies following treatment of intracranial aneurysms with the Pipeline embolization device. Retreatment rates after treatment with the Pipeline embolization device alone versus Pipeline and coil embolization of cerebral aneurysms: A single-center experience. Resolution of mass effect and compression symptoms following endoluminal flow diversion for the treatment of intracranial aneurysms. Unruptured large and giant carotid artery aneurysms presenting with cranial nerve palsy: Comparison of clinical recovery after selective aneurysm coiling and therapeutic carotid artery occlusion. Neurological examination revealed orientation to person and place only, with significant dysarthria and confusion. Sensation was decreased on the left hemibody, with associated neglect of the left upper and lower extremities and a mild left hemiparesis. The most common stroke mimics include seizures, complicated migraines, neoplasms, metabolic derangements, sepsis, and syncope. Seizures, complicated migraines, and syncope can often be ruled out by the clinical history and physical examination. Patients suffering from complicated migraines will typically have a history of migraines, and the acute episode of hemiparesis will usually be accompanied by a severe headache, scintillating scotoma, and/or aura. Symptoms associated with a syncopal episode often overlap with those of a vertebrobasilar stroke, although typically without the cranial nerve findings expected with an ischemic insult to the brainstem. History and physical examination, in addition to cranial imaging, are often sufficient to distinguish between ischemic stroke and stroke-mimicking diagnoses. Seizures: Although a post-ictal paresis or plegia is often seen following a seizure, the majority of patients will present with stereotypical motor movements or paresthesias. Unfortunately, the absence of such movements does not rule out a seizure, nor does their presence confirm diagnosis. Complicated migraines: Migraines may be complicated with either hemiplegia or vertebrobasilar symptoms (ataxia, decreased consciousness, or vertigo). Patients will often have a personal or familial history of migraines, and these episodes are often accompanied by a headache and/or scintillating scotoma. Syncope: Symptoms of syncope may resemble vertebrobasilar ischemia, including loss of consciousness and vertigo. Neoplasm: Intracranial neoplastic processes may present with stroke-like symptoms, such as in the case of seizure, intratumoral hemorrhage, or apoplexy, although presentation is often subacute or progressive. For this patient, the management of symptomatic carotid stenosis is relatively straightforward, although some debate exists regarding the timing and exact nature of treatment. As such, the American Heart Association official guidelines recommend that revascularization for symptomatic carotid artery stenosis should ideally occur within 14 days of an ischemic event. What adjunctive measures can be undertaken to detect potential ischemic complications during the procedure Patients are typically started on 325 mg of daily aspirin prior to surgery, which is continued postoperatively, although some surgeons prefer additional perioperative clopidogrel. Patients are typically placed under general anesthesia and positioned supine with the head rotated slightly away from the operative side. A shoulder roll may assist with a slight degree of extension to increase exposure. A longitudinal incision is fashioned along the anterior border of the sternocleidomastoid muscle. This is carried down through the platysma, and a plane just medial to the anterior border of the sternocleidomastoid is identified and opened further through blunt dissection. A large transverse sensory nerve may be encountered and can be sacrificed to facilitate exposure, although the surgeon should be careful not to violate the parotid fascia. The neurovascular bundle involving the carotid artery can then be easily identified and palpated. Sharp dissection can be used to open the cervical fascia, and then blunt dissection can be performed. Important structures encountered during this exposure include the common facial vein, omohyoid muscle, and hypoglossal nerve. The common facial vein, an anteriorly oriented branch of the internal jugular vein, often lies directly superficial to the carotid bifurcation and should be suture ligated and divided to facilitate exposure. The omohyoid muscle typically marks the inferior extent of the dissection and usually can be left intact. The vagus nerve and its superior laryngeal branch lie deep to the carotid and internal jugular vein, and care must be taken to avoid disruption of these structures when dissection below the carotid is needed. Damage to the superior laryngeal branch of the vagus nerve will result in significant postoperative dysphagia. A shunt can be placed if clamping potentiates changes in intraoperative ischemic monitoring. It is important to start the dissection below the bulk of the plaque and truncate the plaque sharply at the proximal extent of the arteriotomy. Careful inspection of the intima is required to identify any residual debris or plaque material for removal. Particular attention must be paid to the distal end to ensure that no ledge or intimal flap is present because this significantly raises the risk of dissection. If the plaque does not come to a smooth end, it can be sharply cut and tacked down with sutures, although with adequate distal exposure this is rarely required. If tack-up sutures are needed, it is often prudent to employ a patch to obviate the possibility of residual stenosis at the distal end. Alternatively, a patch may be sewn into the arteriotomy site using an autologous saphenous vein or prosthetic material. This maneuver facilitates removal of any air or surgical debris remaining within the lumen. Particular care must be paid to the distal site of the endarterectomy because a residual intimal flap or ledge can become an arterial dissection or the source of postoperative thromboembolism. In patients presenting with symptomatic carotid stenosis of at least 70%, early surgical intervention within 14 days decreases the risk of recurrent ischemic events. Aftercare Postoperative monitoring (including telemetry and blood pressure monitoring) should be performed in the intensive care unit. Strict blood pressure management, typically with a goal of approximately 20% reduction of the baseline blood pressure, is important to avoid cerebral hyperperfusion. Early mobility and ambulation are encouraged the evening of surgery, and nearly all patients can be discharged on the first postoperative day. Sustained elevations in blood pressure should be treated aggressively with intravenous -blockers (labetalol) or vasodilators (hydralazine). A postoperative decline in neurologic status raises concern for a thromboembolic event. An early postoperative deficit or decline in neurologic status demands an immediate response. Traditionally, such patients were returned to the operating room for immediate surgical exploration of the endarterectomy site. More recently, the preference has been to perform cerebral angiography instead, in case thrombectomy is required. When possible, immediate return to the operating room and awake fiberoptic intubation in a controlled setting are preferred. If imminent airway compromise and/or stridor are present, immediate opening of the wound may be necessary, even at the bedside. Once the airway has been secured, surgical exploration of the hematoma and arteriotomy can commence. Strict control of blood pressure in the postoperative setting can avoid cerebral hyperperfusion and potential secondary intracranial hemorrhage. Early and significant postoperative neurologic decline should be addressed with immediate return to the operating room or neurointerventional suite. Postoperative neck hematoma is a neurosurgical and anesthetic emergency, in which securing the airway is of utmost importance. Rarely, opening the wound at the bedside may be a necessary and life-saving maneuver. Cranial nerve deficits, most commonly transient vocal cord paralysis and/or dysphagia, can be seen in approximately 1% of patients, although these are rarely permanent. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis: North American Symptomatic Carotid Endarterectomy Trial Collaborators. Summary of evidence on early carotid intervention for recently symptomatic stenosis based on meta-analysis of current risks. In-hospital stroke recurrence and stroke after transient ischemic attack: Frequency and risk factors. Levy Case Presentation 16 A 77-year-old male with a medical history significant for hypertension, hyperlipidemia, and a coronary artery bypass graft was found to have a right-sided carotid bruit detected on auscultation during physical examination. His previous medical management consisted of lifestyle modifications, aspirin, and statin therapy. He had no referable symptoms, no history of ischemic or hemorrhagic stroke, and no signs of transient ischemic attack. What are appropriate imaging modalities for the evaluation of asymptomatic carotid stenosis Assessment and Planning Carotid stenosis is commonly found incidentally on physical examination during auscultation of the neck that reveals a carotid bruit or during evaluation for possible transient ischemic attacks. The typical modality used in a primary care setting is duplex carotid ultrasound imaging. The systolic and diastolic velocities measured with ultrasound imaging help clinicians judge the accuracy of the percentage. In addition to establishing the percentage of stenosis, clinically understanding the need to treat and the risks and benefits is critical when assessing and advising patients. Since the advent of these trials, medical management has significantly improved with the use of statin and antiplatelet therapies. There is no class I evidence estimating stroke rates associated with current best medical management. Understanding this risk profile will be important for future surgical planning and management for these patients. In addition, there is increasing interest and literature surrounding cognitive decline and its relation to asymptomatic carotid artery disease and whether surgical or endovascular revascularization can benefit cognitive decline. For surgical planning, a detailed understanding of the arterial and venous anatomy and its association to bony landmarks is important. Knowledge of the Circle of Willis helps one to distinguish sources of blood supply to the hemisphere ipsilateral to the stenosis. This allows a better understanding of potential collateral routes during clamp time while performing carotid endarterectomies. Physical examination and routine Doppler ultrasound studies are useful in screening for an underlying asymptomatic carotid stenosis. Cerebral angiography helps elucidate many different anatomical aspects of a carotid lesion, including the following: a. Which other key radiographic features would increase the risk of periprocedural stroke Which studies can help differentiate plaque morphology and the likelihood that plaque is actively generating thromboemboli Which radiographic features can help determine the possible need for intraoperative shunting Decision-Making After diagnosis, initiating the best medical therapy, including antiplatelet therapy, statin therapy, and lifestyle modifications, is warranted. The 4-year rate of stroke or death among asymptomatic patients between the stenting group and the endarterectomy group was 4. The patient in this case did not have high-risk features such as a lesion extending above C2, a neck with difficult access secondary to adipose tissue and other anatomical constraints, previous neck surgery. Surgical Procedure the current patient underwent routine preoperative evaluation and assessment, including medical clearance from his primary care physician. It is important to avoid overt hypotension during induction of the anesthesia to prevent hypoperfusion prior to surgery. The patient is positioned supine with the head slightly extended at the neck and chin and slightly rotated toward the opposite side of the lesion. The platysma is split and undermined both above and below the incision to allow adequate exposure. The digastric muscle is exposed proximally; the omohyoid muscle is exposed distally.

By comparison prostate cancer years to live , when the pacing electrode is at the tip man health daily relationships category , the electrode may contact the myocardium without being wedged prostate cancer x-ray images . There are a variety of approaches to passive fixation man health clinic , including tines (straight) prostate oncology quotes , single curve prostate cancer prevention , double curve (S-shape)58,59 and double cant. Nof and colleagues found no significant differences in success or complication rates among passive fixation leads. If lead selection is limited to one manufacturer, a less desirable target vein or even implantation failure may result. Jude, Biotronik, and Sorin (Milan, Italy) have unique preformed distal shapes intended to promote stability and orient the tip electrodes toward the myocardium. Type, Size, and Personality of Left Ventricular Pacing Lead Each lead has a size, shape, and electrode configuration that produces a "personality" that will have advantages and disadvantages when the lead is used in different veins. The section in this book on commercially available leads gives examples of how changing the method of lead fixation can solve problems of lead instability, high thresholds, and phrenic pacing. Selecting the Shape of the Vein Selector As mentioned previously, the current approach relies on the shape of the vein selector and not the delivery guide for target vein cannulation, which is now possible because of the soft tip on the vein selectors and the delivery guide. The black distal section of the catheter is soft and can be easily straightened as it is advanced over wires into the target vein. Thus, once the ostium of the vein is identified by a puff of contrast, the wire can be advanced followed by the vein selector to add a second wire. The ability of the vein selector to be advanced deep into the vein over the wires allows for the creation of a stable rail over which to advance the delivery guide. Selecting the Lumen Size of the Delivery Guide the size of the lead suitable for the target vein determines the lumen size of the delivery guide to be used. The soft tip section of the delivery guide can be advanced deep into a target vein over the vein selector if needed. As a result, we now rely on the shape of the vein selector and not the shape of the delivery guide to accommodate the takeoffs of various veins. When looking for the target vein with the vein selector, proper interventional technique must be used. Ideally, puffs of contrast are only used to verify position but may be necessary to reveal the target vein location. Remove the Vein Selector Retaining the Wires and Deliver the Lead It is particularly important that the instrument table be perpendicular to the patient table as the vein selector is withdrawn. To prevent the delivery guide from being displaced during the process of removal, it is important not to advance the wires as the vein selector is removed. To maintain wire access in the vein, it is important not to pull the wires out as the vein selector is removed. Keeping the wires in a stable position during the process is best accomplished with the catheters in a straight line resting on the table. Once the lead is in place, it is time to discuss removing the delivery system without displacing the leads. There are several factors that influence the risk of lead dislodgment during removal of the guiding catheter. The use of a delivery guide impacts lead dislodgement via the size and final position of the lead. Use of a delivery guide impacts lead dislodgment via the final position of the stylet. Final Lead Size and Position A delivery guide helps insert a lead that is appropriately sized and positioned in the vein which is less likely to be displaced. With large veins, a 9-Fr delivery guide allow larger (6- to 7-Fr), more stable leads to be placed compared with the smaller, 6- to 7-Fr delivery guides (4- to 5-Fr leads). B, Injection system is attached to the vein selector through a rotating Y-adapter. Again,tousetheveinselector in a safe and effective manner and to reduce contrast use, both handsmustbeonthecatheter. Slicing Versus Peeling for Coronary Sinus Catheter Removal Slicing requires the operator to fix the lead to the slicer, fix the position of the slicer and lead, then pull the catheter straight back over slicer without moving the cutting hand or allowing the lead to lead to buckle or detach from the slicer. A natural tendency is to pull the catheter off to one side, disengaging the blade from the catheter. If the lead is not dislodged as the blade disengages, the motion of trying to reengage the blade into the catheter frequently does dislodge it. If additional lead slack is required to prevent lead dislodgement, it cannot be added (fixed slicing hand position) until the slicing operation has been completed. Before peeling, an assistant stabilizes the lead distally by pinching the walls of the sheath against the lead where the sheath exits the body. With the lead secure, the hub is cracked and the sheath peeled down to the fingers of the assistant. The cycle of withdrawal, pinch, and peel is repeated until the sheath clears the body and the assistant can secure the lead. The sliceable plastic hub is joined to the braided catheter via an overlapping of the plastic and braid. The resistance to cutting increases significantly as the blade reaches the plastic hub and then decreases abruptly as the blade reaches the guide. The telescoping delivery guide supports the lead in the target vein while the angioplasty wire is removed and the stylet is advanced. The importance of using a soft curved stylet becomes apparent once guides and sheaths are removed. Usingthe support provided by the vein selector and wires, the delivery guide is advanced toward the ostium of the target vein. B, Support provided by the extrasupport wire and the delivery guide allows the lead to be advanced deepintothesmallvein. Thesheathdetermines the length of the lead in the body, particularly in the right atrium. Pressure Products achieves this by exposing the catheter when the valve is broken in two pieces. Jude have integrated, slittable hemostatic hubs where the troublesome transition between hub and guide is avoided. Splitting the Hub/Guide Without Grabbing and Displacing the Lead After it is cut, the thick plastic of the hub of the guide can close around the lead. B, Without moving the lead, the operator cuts the third-generation guide down to the SafeSheath hub. The operator removes the lead from the cut guide and secures it to the cutter by placing the lead in the notch of the cutter under thethumb. C D Pinching the lead between the walls of the sheath stabilizes the lead and sheath distally. Because there is no braid, the walls of the sheath can be pinching against the lead reducing blood loss and the risk of air embolization once the valve is removed. It is far more difficult, if not impossible, to effectively pinch a catheter with wire braid incorporated in the wall. After an assistant releases the sheath/lead, the rest of the sheath is drawn back over the lead under fluoroscopic observation. As the tip of the sheath exits the body and the pacing lead becomes visible, the assistant secures the lead position with fingers in the pocket. The two issues of importance are the physical characteristics of the stylet and how the stylet is withdrawn. An unsupported lead with a stylet may result in the tip of the lead withdrawing from the target vein. A softer stylet exerts less displacing force when the shape of the stylet and course of the lead do not match despite the curve. The longer the stylet remains in a position prone to displacing the lead, the more likely the lead will be displaced. To prevent the stylet from displacing the pacing lead when the course of the lead and the shape of the stylet do not match, the stylet is removed quickly (like pulling the cord on a lawn mower). Consider a comparison of the relative risk of arterial to venous system complications. In an artery, the blood is under high pressure and will extend the dissection under the flap. After a venous perforation, there is a very small pressure gradient between the venous blood and the pericardial space. Highpressure and the direction of blood flow in the artery (arrows) will lift the flap andextendthedissection. However, the effect of catheter-induced trauma resulting in closure of a venous structure is of no acute or long-term significance other than the lack of venous access. Longer procedure times potentially increase problems with sedation and the risk of infection. Contrast stains that develop with the use of open-lumen catheters initially caused great concern frequently with termination of the procedure. In fact, contrast stains are clues and when identified quickly, indicate a misstep that can be corrected before significant damage occurs. Use of contrast material identifies the "catheter" location at all times, limiting unintentional trauma. When contrast material is injected with the balloon inflated, the distal pressure increases, further forcing blood and contrast material into and through the venous disruption. A, Medtronic Attain 6218 guide is advanced over a wire and small catheter (second-generation telescoping system) into the lateral wall target vein. D, Lead is removed, and contrast material is injected into the posteriorlateralvein. SafeSheath sealing adapter is press-sealed into the hub and removed by cracking the hub into two pieces (Pressure Products). To make best use of the new delivery systems, physicians need to develop interventional skills that leverage these tools. With use and changes in catheter design, our understanding of how delivery guides are best used has evolved. When the tips were stiff, it was necessary for the shape of the delivery guide to match the vein takeoff. With use, we found that despite specific shapes, a small catheter was frequently required to locate the vein and serve as a rail to advance the guide into the vein, that is, the vein selector. The size, shape, and flexibility of the new vein selector is better suited to deal with difficult vein takeoffs than the delivery guide. With the vein selector responsible for locating and providing a rail, only one shape of delivery guide is necessary. Acuity Steerable the Acuity Steerable is the only Boston Scientific lead with an electrode at the tip. The J can be partially straightened with a style to help direct or steer the lead. To open the valve to admit a lead or another catheter, the valve is compressed(black arrow). The catheters are designed for delivering the Attain Ability Lead with a 4-Fr lead body but a maximumdiameter5. The small French size and tapered distal tip make it useful for small veins and retrograde placement through collaterals. With these leads, it is often difficult or even impossible to find a suitable location in a large target vein because of diaphragmatic/phrenic stimulation distally, with high pacing thresholds and lead instability proximally. Once at the desired location, the wire is removed and the lead resumes a helical shape, securing it in place. Because of the helical design, a larger surface area of lead is in contact with the vessel wall. If high pacing thresholds or phrenic pacing are encountered at a specific site, the lead can be straightened and moved proximally or distally. There are two bipolar leads (Attain 4194 and the Attain Ability 4196) and one unipolar lead (Attain StarFix). The distance between the distal and proximal bend influences the final position of the lead in the vein. If the lead is advanced or withdrawn slightly (2-4 mm) to avoid phrenic pacing or high thresholds, the lead tends to return to its original position. The double cant method of fixation is also prone to migrate proximally if the target vein is large or if the proximal bend is not within the target vein. The more acute angles of the Attain Ability were designed to reduce the propensity for proximal migration. The Attain StarFix is designed to eliminate migration with lobes that when deployed wedge into the vein. The lead body is 2 mm with outer polyurethane insulation and inner silicone insulation. The double cant shape is designed to direct the tip toward the myocardium and stabilize the lead in the target vein. Even with favorable venous anatomy, at times it is difficult to advance the Attain 4194 sufficiently to achieve stability. If the tip or anode coil meets resistance, the lead may not advance far enough to be stable. After several attempts with different wires, however, the lead retracted after the wire was removed. Only with the support of a delivery guide was the lead advanced to a stable position. This is another example where starting with a vein selector and delivery guide, even when it appears that lead placement will be easy, would have saved time.

Voltage is the potential energy per unit charge for a charged object in an electric field man health magazine . Because voltage is potential energy per unit of charge prostate cancer xenograft models , it is measured in terms of joules/coulomb prostate cancer medscape , as follows: 1 volt = 1 joule coulomb When one refers to "voltage prostate cancer and diet ," the reference is to a difference in potential between two points in space prostate cancer gleason score 9 . Although electric charge may move through several mechanisms prostate 0270-4137 , for clinical purposes, electric charge is usually carried by the flow of electrons through a wire. By historical convention, current is considered to flow in the direction that positive charges would move. In reality, however, an electric current in a wire is carried by the movement of electrons that are negatively charged. For clarity in this chapter, current is stated in terms of electron or ion motion. Because electric current is the movement of charge, it is measured in terms of coulombs per second (It = dQ/dt), with 1 ampere of current equal to the movement of 1 coulomb/sec. For lithium-iodine batteries at beginning of life, the chemical reaction generates approximately 2. The total amount of charge that is available in the battery is measured in terms of the amount of current that can be provided multiplied by the duration that the current can be sustained. The activation map is shown as a color contour map and is superimposed on a grayscale image of the model, which in turn, is superimposed on a photograph of the preparation. Note the earliest activation in blue with rapid spread of activation in the cranial direction toward the bundle of His. The difference in voltage between the anode and cathode in the battery results in a flow of charge (current) from the pulse generator through the conductors in the leads, electrodes, extracellular electrolytes, cell membranes, and intracellular ions and charged molecules. In other words, the voltage drop across each element in the circuit must sum to the total potential difference across the entire circuit. Thus the electromotive force (voltage) generated by the battery (an increase in potential energy) must be completely dissipated (a decrease in potential energy) as current flows through all the elements of the circuit to end at the battery. Electric circuits in the clinical practice of pacing have multiple elements, including the pulse generator battery, the lead conductor(s), the electrodes, the myocardium, and blood within the great veins and cardiac chambers. Thus the current flowing through all elements in series is the same, with the voltage difference decreasing sequentially as it passes through each element in the circuit. Therefore the potential difference is the same before each element and after each element, and current will flow from one of the common conductors to the other through any or all of the elements. The quantity of current flow in each element is inversely related to the factors that oppose the flow of electric charge in that element. Most biologic circuits are made of various combinations of series and parallel modules or subcircuits. For example, because of electrochemical effects, an electrode placed in the heart may act as a capacitor in parallel with a resistor, both in series with the lead joining the pulse generator to the electrode. Electrons from the pulse generator flow through the cathode-tissue interface and return to the anode, which may be located on a pacing lead or the pulse generator casing. The terminology used for electrode polarity may seem confusing as applied to lead electrodes and the electrodes of a battery. The battery anode, by continuing oxidation becomes positively charged (Li+) while furnishing electrons to the circuit external to it. Therefore the terminal of the battery where electrons are provided to the circuit is the battery anode. From the battery anode, electrons are conducted through circuitry in the pulse generator and eventually enter the pacemaker lead, where they are conducted through the conductor to an electrode that is in contact with the myocardium. This electrode, receiving electrons from the pulse generator and furnishing electrons to the tissue, is the lead cathode. The return electrode located more proximally on a lead within the heart or on the pulse generator casing is the lead anode. It collects electrons from the tissue and returns them through the pulse generator circuitry to the positive electrode of the battery, the battery cathode, where reduction occurs. The consistency in the terminology is that, when oxidation occurs, it occurs at an anode, and in the circuitry, an anode connects to a cathode that subsequently connects to another anode, and so on. As current flows through some of these elements, such as conductor wires in the leads, the opposition to current flow results in energy being lost as heat. These elements are known as ohmic, and the opposition to current flow is called resistance (R). The instantaneous voltage developed across a perfect resistor is linearly proportional to the instantaneous current flow through the resistor. In order for conduction to occur from the electrode to the tissues and blood pool, electron motion in the lead wires and electrodes is converted to ion motion in the interstitial fluid. However, during the duration that the pacing stimulus is applied, there develops increasing charge on the capacitor resulting in increasing opposition to further current flow from the start to the end of the stimulus. Impedance can be defined as the vector sum of all forces opposing the flow of current in an electric circuit. Impedance has a magnitude and a phase angle, both dependent on the rates of change of the applied voltage. The phase angle represents the difference in timing of sinusoidal current flow peaks compared with sinusoidal voltage peaks when a sinusoidal voltage is applied to a circuit. Because a negatively charged pacing electrode in contact with the endocardium is surrounded by blood and interstitial fluid, positively charged ions move toward that electrode during a pacing stimulus. This is time-dependent and results in the phenomenon of polarization, which develops rapidly as the stimulus is applied and dissipates slowly after the end of the stimulus. This effect of ions moving to oppose the flow of electric current has the effect of a capacitor in the circuit. A capacitor is an object that stores energy in an electric field by holding positive charges apart from closely approximated negative charges. A capacitor requires a material or space between the layers of negative and positive charges that is normally nonconducting (the dielectric). A cell membrane, although leaky, acts as a capacitor by separating the negatively charged inside of the cell from the more positively charged outside. The interface between a pacing electrode and the charged electrolytes that surround the electrode at its surface in the myocardial tissue acts, in part, as a capacitor. The terms Helmholtz capacitor and Helmholtz capacitance are used in this chapter for capacitor-like effects that occur at pacemaker and defibrillator electrode-electrolyte interfaces. Capacitance (C) specifies, for a given voltage applied across a capacitor, how much electrical charge (Q) can be stored by the capacitor. One farad is the capacitance of a capacitor that, on being charged to 1 volt, will have stored 1 coulomb of charge (the amount of charge delivered by 1 ampere flowing for 1 second). A voltage or current pulse of any shape can be broken down mathematically into combinations of sinusoidal components. They store or release energy in or from an electric field (capacitor) or a magnetic field (inductor). If a sine-wave voltage is applied to a pure capacitance, the current peaks occur 90 degrees earlier than the voltage peaks. If a sine-wave voltage is applied to a pure inductance, the current peaks occur 90 degrees later than the voltage peaks. The total reactance in a simple series circuit is the scalar sum of the inductive and capacitive elements, each of which varies with the frequency content of the applied signal. Impedance also varies with signal frequency; it is the vector sum of reactance and where Qt is the total charge delivered between time 0 and time t, and it is the instantaneous current at each time segment between time 0 t and time t. An inductor is an object that stores or releases energy in or from a changing magnetic field. The voltage difference across an inductor is proportional to the rate of change of current flowing through the inductor. Energy is stored during the formation of the magnetic field and is released when the magnetic field decreases or disappears. Inductance is the term that specifies the relationship between the voltage across an inductor and the rate of change of current traversing the inductor. Cell membrane currents have some of the current- and voltage-versus-time characteristics of an inductance in parallel with a capacitance. Pure reactance values depend on the rates of change of current and voltage, whereas pure resistance values do not. The component of reactance that is most relevant to both pacing electrodes and cell membranes is capacitance, with inductance being much less important. For example, the cardiac action potential spreading throughout the heart generates a changing magnetic field that transiently stores a very small amount of energy. However, the changing magnetic field generated by spread of the action potential is so small that it is not clinically significant except in the research setting. C these equations indicate that, for an instantaneous current it, the instantaneous voltage across the series circuit is the sum of the effects at that instant in time of the resistance, capacitance, and inductance of the circuit. Note especially that the instantaneous effects are highly in the capacitor from time 0 to the instantaneous time t. The equations show that the capacitance effect on the voltage decreases as the capacitance increases. Thus the polarization voltage that produces afterdepolarizations in the electrogram immediately following a pacing stimulus decreases as the electrode capacitance increases. This is especially relevant for automatic capture algorithms which rely on the accurate detection of an evoked response to assess whether capture has occurred. These (and more complicated charge redistributions) occur because of attraction and repulsion interactions between an electrode held at a given electric potential. The charge placed on the electrode, by electrostatic attraction, forces the accumulation of a polarized water layer and a second layer of hydrated, oppositely charged ions adjacent to the electrode surface. The Helmholtz model does not take into account other factors, such as absorption on the surface, thermal buffeting, and interaction between solvent dipole moments and the electrode. Models more complicated than the Helmholtz include the Gouy-Chapman and Gouy-Chapman-Stern. In a semiconductor or in localized regions of an electrolyte, an excess of positive or of negative charge may be present. If the excess is of positive charge carriers, the positive carriers are the majority carriers and the negative charge carriers the minority carriers. An excess of negative carriers makes these the majority and the positive carriers the minority. In physiologic electrolytes, the ions include Na+ and Cl- in major concentrations (majority carriers). The ions attracted to or repelled from the electrode during the electrical stimulation pulse make up a separation of charge in the tissue electrolyte. When the pacemaker pulse is applied as a negative voltage to the electrode, electrons accumulate in the electrode. Reversible reactions may form metal-oxide complexes on the surface of the electrode. Positive ions surrounded by water molecules-a water shell-make a secondary water layer. This accumulation of positive ions in the electrolyte near the electrode unbalances local electrolyte charge neutrality. Secondary ion rearrangements occur in great complexity, with several names for the various processes. When the pacemaker pulse stops, the ions that have accumulated, being no longer attracted to or repelled from the electrode, gradually rearrange themselves back toward their original, electrically neutral position. Ion rearrangement is not as fast as the transmission of an electric potential in a wire. The decaying voltage gradient in the tissue persists long enough to be detected by a pacemaker or defibrillator and may be great enough to interfere with sensing in autocapture devices in some situations. First, oxidation-reduction reactions, which can be reversible or irreversible, involve electron movement across the interface and constitute faradic current. The second process, nonfaradic current, occurs without transfer of electrons across the interface. It consists of electron flow in or out of the electrode itself and a flow of ions in various layers or "clouds" toward or away from the interface. This nonfaradic process is similar to charging or discharging an electrical capacitor, but at the surface of an electrode in electrolyte there is directed electron drift in or out of the electrode and directed ion drift within the electrolyte. The ion flow and the electron flow each constitute an electric current; yet no charge crosses the interface. Away from the electrode in the body of the electrolyte, the electric potential gradient causes ions to move away from or toward the electrode region, depending on their charge. Ion mobility characteristics, concentration gradients, and temperature gradients also affect ion movement. In the heart the process is more complicated than in an electrolyte solution alone, because of the anisotropic properties of the extracellular and intracellular domains. Whether electron transfer across the interface occurs depends on the properties of the electrode and the electrolyte and on the applied electric pulse characteristics. The current crossing the interface when one is charging a battery is faradic current produced by oxidation-reduction reactions. Capacitance current flow is the accumulation of charge on the electrode at the interface balanced by a corresponding accumulation of charge of net opposite sign in the electrolyte adjacent to the interface. The flow of charge into the capacitor is measurable current in a pacemaker lead, even though in a perfect capacitor, no charge crosses the interface. The resulting arrangement of ion groupings at and near the electrode-electrolyte interface can be very complicated. When a pacemaker pulse is applied to an electrode in the heart, the charge movement into or out of the Helmholtz capacitance-both electrons in the electrode and ions in the electrolyte-is an electric current, even though no charged particle necessarily crosses the interface. It is dependent on current density, electrolyte composition, and the area and other surface characteristics. This voltage response between phases is a function of the rates of ion movementintheelectrolyte. Another approach to minimize polarization is to abruptly reverse the polarity of a pacing stimulus during the pulse (biphasic pulses). When biphasic pulses are used, minimal postpulse polarization persists, provided the time between phases is in the microsecond range.

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