Real-time frameless localization can be achieved by replacing the stereotactic frame with rigidly attached skull markers (“fiducials”) that provide a fixed reference selegiline 5mg with amex. Another innovative alternative is to produce a custom- made fixed trajectory guide using rapid prototyping techniques discount 5 mg selegiline free shipping. Both of these approaches have been used successfully and appear to be equivalent in accuracy to a stereotactic frame buy selegiline discount. In one approach, the target is confirmed by assessing symptomatic resolution during high-frequency macrostimulation and by identifying surrounding structures using their characteristic stimulation-evoked responses. In the other approach, before stimulation testing, single-neuron recordings are performed to localize the appropriate target through somatotopic kinesthetic and/or somatosensory responses. In an awake patient, appropriate stimulation is delivered to the skin or by passive and active movement of the joints. Anesthesia or sedation can modify neuronal activity significantly and, thus, interfere with functional mapping. For example, propofol has been shown to inhibit globus pallidus and subthalamic neurons for several minutes beyond its behavioral effects. Tremor syndromes are treated by targeting the ventral intermedius thalamic nucleus (thalamotomy or stimulation), whereas dystonias are treated by stimulation of the globus pallidus interna. Abrupt loss of intrathecal infusion of baclofen, however, can quickly lead to a serious withdrawal syndrome with dysautonomia, circulatory collapse, and death within hours. Spasticity refractory to intrathecal baclofen may be amenable to selective dorsal root rhizotomy performed through an open laminectomy. Anatomical locations for therapeutic lesions (thalamotomy and pallidotomy) for the surgical treatment of Parkinson’s disease. Inset shows the plane of the coronal section through the diencephalon, identifying the lesions. A 2–3 cm linear incision (burr-hole access) or stab wound (twist-drill access) generally is placed near the coronal suture and 10–50 mm from the midline in the frontal bone. Subsequently, minimal or no sedation is used, as patient cooperation is necessary during the functional mapping component of the case. If single-neuron recordings are used, propofol should be discontinued at least 20 min in advance of mapping because it can produce prolonged suppression of target neuronal activity. To enhance single-cell responses, withhold medications prescribed for target symptoms for 8–24 h. To facilitate intubation, the calvarial wound is closed temporarily, and the stereotactic localizing apparatus is removed. Closure consists of a single, interrupted suture for stab wounds or two-layer suture/staple closure for a burr hole. The subcutaneous layer is closed with absorbable sutures, and the skin is closed with staples or sutures. It is caused by the loss of dopaminergic neurons in the substantia nigra → ↓ dopamine (dopamine/acetylcholine imbalance) in basal ganglia → movement disorder. Medical treatment also may include dopamine agonists (pergolide [Permax]; bromocriptine [Parlodel]), and acetylcholine antagonists (amantadine [Symmetrel], benztropine [Cogentin]) to correct the dopamine/acetylcholine imbalance. They will have been taken off their antiparkinsonian medications 8–24 h before surgery. This will maximize their symptoms to help assess treatment effects intraop; thus, preop assessment on the day of surgery will be difficult. Deuschl G, Schade-Brittinger C, Krack P, et al: A randomized trial of deep-brain stimulation for Parkinson’s disease. Fasano A, Daniele A, Albanese A: Treatment of motor and non-motor features of Parkinson’s disease with deep brain stimulation. Joint C, Nandi D, Parkin S, Gregory R, Aziz T: Hardware-related problems of deep brain stimulation. Krack P, Fraiz V, Mendes A, et al: Postoperative management of subthalamic nucleus stimulation for Parkinson’s disease. It can involve both neuropathic and nociceptive processes and occur in a variety of anatomical distributions (e. Therapeutic interventions are dictated by the pathophysiology of the pain, its qualitative nature, etiology, and the patient’s prognosis. Many common procedures for chronic pain are directed at the spinal cord and may consist of epidural or intrathecal medications or electrical stimulation. Percutaneous electrodes are easier to implant and have less associated surgical pain. The surgical electrode (implanted via laminectomy) confers greater mechanical stability in the epidural space. In addition, given its larger contact size, it can generate higher current densities with less drain on the implanted system. For percutaneous electrodes, a small skin incision is made two to three vertebral levels caudal to the target region of the spinal cord. For “surgical paddle” electrodes, the skin incision is made one to two levels caudal to the target zone of the spinal cord, and a laminectomy is performed to provide access to the epidural space. Most percutaneous electrode placements and some paddle electrode placements are done awake so that intraoperative test stimulation can be performed. The procedures are done in the prone or lateral position with consequent implications for airway management in the sedated patient. Localization of the electrodes is accomplished initially based on radiographic criteria; however, these localizations are only approximate, and it is recommended that the electrode placement be confirmed by intraop stimulation. The patient needs to be sufficiently alert to communicate the quality, distribution, and intensity of the stimulation-induced paresthesias. Surgical paddle placement requires a variable extent of muscle dissection and laminectomy, which may be done under general anesthesia or with epidural anesthesia for patient comfort. If done under general anesthesia, response to paddle test stimulation may be measured by manual palpation of musculature stimulated at higher test voltage, and/or using intraoperative electrophysiologic monitoring. To assess efficacy, the electrode may be externalized and percutaneous stimulation used for assessment. Postop, these patients can have an exacerbation of pain, particularly if neuropathic in nature. They may require iv lidocaine or ketamine infusions to return them to their preop baseline, even with a functioning and appropriately located stimulating electrode. Thalamic interventions include stereotactic insertion of stimulating electrodes into sensory thalamus. For medically intractable neuropathic pain syndromes, epidural motor cortex stimulation has shown mixed results. The incision consists of a 5–10 cm linear or 5 × 10 cm trapezoidal incision placed over and paralleling the motor cortex. In rare cases, the surgeon may elect to perform the surgery awake to facilitate mapping. To assess efficacy, the electrode may be externalized and percutaneous stimulation assessed for overall therapeutic efficacy. The mainstay of surgical treatment of trigeminal neuralgia is microvascular decompression of the trigeminal nerve in the prepontine cistern (see p. Stereotactic radiosurgical techniques are increasingly utilized as an ablative treatment for trigeminal neuralgia, particularly in the elderly (> 65 yr old) population or in other surgically averse candidates.
These are described further elsewhere and may include the Borg Scale of Perceived 1 Exertion cheap selegiline 5mg on line. Electrocardiographic Lead Systems As the technology of exercise electrocardiographic testing has evolved generic selegiline 5mg with amex, several different types of lead systems have been developed and used buy discount selegiline on line. Details regarding these lead systems, along with skin preparation 1,3 techniques, are provided elsewhere. Torso electrodes are placed under the lateral aspect of the clavicles for the arm leads and on the lower end of the rib cage or high under the rib cage for the leg leads. Several exercise test protocols are available for both treadmill and stationary cycle ergometers. Patients who have low estimated fitness levels or are deemed to be at higher risk because of underlying disease (e. Ramp protocols are designed with stages that are no longer than 1 minute and for the patient to attain peak effort within 8 to 12 minutes. Because there are no widely published or standard sets of ramp protocols, individual exercise testing laboratories usually develop their own customized protocols that accommodate a wide range of fitness 4,5 levels. Symptom-limited tests are designed to continue until the patient demonstrates signs and/or symptoms necessitating termination of exercise (Table 13. Whatever modality or protocol is used, standard patient monitoring and measurements are made during and early after exercise (Table 13. Exercise standards for testing and training: a scientific statement from the American Heart Association. A period of active cool-down may be included in the recovery period, particularly following high levels of exercise, to minimize the postexercise hypotensive effects of venous pooling in the lower extremities. Patients should be observed until all symptoms have resolved or returned to baseline levels. Cycling may be preferable when orthopedic or other specific patient characteristics limit treadmill testing or during exercise echocardiographic testing to facilitate acquisition of images at peak exercise. From American College of Sports Medicine Guidelines for Exercise Testing and Prescription. During treadmill exercise, patients should be encouraged to walk freely and use the handrails for balance only when necessary. When precise determination of oxygen uptake is necessary, such as assessment of patients for heart transplantation (see Chapter 28), evaluation by expired gas analysis is preferred over estimation (see Cardiopulmonary Exercise Testing). However, stationary cycling may be unfamiliar to many patients, and its success as a testing tool is highly dependent on patient skill and motivation. Electronically braked cycle ergometers automatically adjust external resistance to the cycling speed to maintain a constant work rate at a given stage. Electronically braked cycle ergometers allow simple programming of ramp protocols. As with treadmill ramp protocols, customized cycle ergometer ramp protocols that accommodate a wide range of fitness levels need to be established by individual exercise testing laboratories. From American College of Sports Medicine Guidelines for Exercise Testing and Prescription. Arm ergometry is an alternative method of exercise testing for patients who cannot perform leg exercise. Although this test has diagnostic usefulness, it has been largely replaced by nonexercise pharmacologic stress techniques. The 6-minute walk test can be used as a surrogate measure of exercise capacity when standard treadmill or cycle testing is not available. It is not useful in the objective determination of myocardial ischemia and is best used in a serial manner to evaluate changes in exercise capacity and the response to interventions that may affect exercise capacity over time. Measurements • Assemble all necessary equipment (lap counter, timer, clipboard, worksheet) and move to the starting point. Patient Instructions Standardized scripted patient instructions should be used, and are provided elsewhere. Peak V̇O2 is the most accurate measure of exercise capacity and is a useful reflection of overall cardiopulmonary health. Measurement of expired gases is not necessary for all clinical exercise testing, but the additional information can provide important physiologic data that can be useful in both clinical and research applications. Use of these variables in graphic form provides 6,8 further information on the ventilatory threshold and ventilatory efficiency. Such testing can provide useful information for differentiating cardiac from pulmonary limitations as a cause of exercise-induced dyspnea or impaired exercise capacity when the cause is uncertain. The personnel involved in administering and interpreting the test must be trained and proficient in this technique. In 2014 these recommendations were updated to define 11 further the roles of each staff member involved with exercise testing. Common to every guideline is the recommendation that patients be screened before exercise testing to assess their risk for an exercise-related adverse event so that the most appropriate personnel to supervise the test can be provided. In all such cases the physician should be immediately available to assist as needed (i. Nonetheless, the safety of exercise testing is well documented, and the overall risk for adverse events is quite low. Maintenance of appropriate emergency equipment, establishment of an emergency plan, and regular 3 practice in carrying out the plan are fundamental to ensuring safety in an exercise testing laboratory. Exercise Testing in Coronary Artery Disease Exercise-Induced Sym ptom s Any chest pain produced during the exercise test needs to be factored into the exercise test conclusion and report. First, are the symptoms reported during the test the same or similar to the reported historical symptoms that prompted the exercise test? If the answer is no, differences between the produced and historical symptoms need to be clarified. In addition, the symptoms produced need to be categorized according to whether they are consistent with angina. Distinguishing anginal from nonanginal chest pain is important at the time of occurrence of the chest pain. Angina is not well localized, pleuritic, or associated with palpable tenderness (see Chapters 56 and 61), and the only opportunity to define these qualities may be after the exercise test. Consideration of limiting versus nonlimiting chest pain, in addition to any induced angina, has been incorporated into the Duke treadmill score, as well as into other treadmill scores (see later). These factors will have an impact on the prognostic and diagnostic assessment of the test results and ultimately the next step in the clinical evaluation. Lastly, if the patient stops exercise earlier than anticipated because of dyspnea, careful consideration should be given as to whether an anginal equivalent is present. If the presenting symptom was dyspnea with exertion, this becomes even more relevant.
Therefore purchase selegiline 5mg visa, careful attention to family and other caregivers is an important 50 part of the end-of-life process buy selegiline 5mg with visa, including grief counseling services after bereavement cheap 5 mg selegiline with mastercard. The Site for the End of Life An important component of end-of-life care planning is to determine where the patient and family anticipate that the final days should occur. Home hospice care includes extended availability for calls and visits to help with symptoms and events at the end; however, dying at home requires continuous support from family or friends, which is not always possible or desired. Inpatient hospice is limited in most areas and usually entails substantial costs not covered by insurance. Alternatively, some end-of-life services can be provided in a long-term skilled nursing facility. Patients who are receiving high-intensity therapies are generally not eligible for home hospice or transfer to a skilled nursing facility. For example, intravenous inotropic infusions or dialysis can be substantial obstacles to peaceful end-of-life care. In these situations, the high level of support must usually be stopped before discharge, in full recognition that death may occur in the hospital. Regardless of the anticipated course, it is always prudent to have a “plan B” to implement if the patient planning to die in the hospital does not do so quickly, or if the patient planning to die at home or his family faces unanticipated difficulties. Smoothing the transition between “do everything” and “do nothing except for comfort” requires attention to what happens in between, after recognition that survival is limited. If the shift in focus from maximizing survival to enhancing quality of life has been successful—minimizing symptom burden, enhancing meaningful interactions, and encouraging achievement of short-term goals—patients and families will often seek to prolong the duration of this phase of “quality survival” before hospice care is indicated. Additional content is available in the online supplement for this chapter (Changing the Culture of Palliative Care). As providers, we need to develop a responsive model of care that honors patient and family goals, as well as stewardship of finite resources, throughout their journey with cardiac disease. Decision making in advanced heart failure: a scientific statement from the American Heart Association. Palliative care and cardiovascular disease and stroke: a policy statement from the American Heart Association/American Stroke Association. Engaging heart failure clinicians to increase palliative care referrals: overcoming barriers, improving techniques. Effect of palliative care–led meetings for families of patients with chronic critical illness: a randomized clinical trial. Proposed policy, payment, and quality provisions changes to the Medicare Physician Fee Schedule for Calendar Year. A survey of clinician attitudes and self-reported practices regarding end-of-life care in heart failure. Development of the Serious Illness Care Program: a randomised controlled trial of a palliative care communication intervention. Conversations in end-of-life care: communication tools for critical care practitioners. Examining the terror management health model: the interactive effect of conscious death thought and health-coping variables on decisions in potentially fatal health domains. Discordance between patient-predicted and model-predicted life expectancy among ambulatory patients with heart failure. Investing in deliberation: a definition and classification of decision support interventions for people facing difficult health decisions. Advanced (stage D) heart failure: a statement from the Heart Failure Society of America Guidelines Committee. Outcomes After cardiopulmonary resuscitation among patients hospitalized with heart failure. Cardiovascular health: the importance of measuring patient-reported health status: a scientific statement from the American Heart Association. Symptom burden, depression, and spiritual well- being: a comparison of heart failure and advanced cancer patients. Clinical characteristics and outcomes of intravenous inotropic therapy in advanced heart failure. Safety and benefit of discontinuing statin therapy in the setting of advanced, life-limiting illness: a randomized clinical trial. Drugs that may cause or exacerbate heart failure: a scientific statement from the American Heart Association. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Short-term opioids for breathlessness in stable chronic heart failure: a randomized controlled trial. Depression as a risk factor for poor prognosis among patients with acute coronary syndrome: systematic review and recommendations: a scientific statement from the American Heart Association. Cognitive behavior therapy for depression and self- care in heart failure patients: a randomized clinical trial. Assisting the bereaved: a systematic review of the evidence for grief counselling. Removing Therapies and Futility Deactivation of Cardiac Rhythm Devices 1 Decisions around withdrawal of therapies are often more complex than the decisions to start them is. In end-stage heart disease, dilemmas arise around deactivation of cardiac implantable electronic devices. Turning off the defibrillator function should be presented as a simple step that may be consistent with the goal of preserving quality of life during the dying process. Although this option relates to resuscitation preferences, patients often have strong and disparate views on external and internal defibrillation. In difficult situations, consultation with 6 palliative care can help clarify the relationship of the device to goals of care. Planned replacement of the device generator at battery end of life should be carefully reviewed in the context of patient preferences, illness trajectory, and reliance on pacing and cardiac resynchronization therapy. Futility Certain therapeutic options may be considered unreasonable or become impossible for an individual patient and therefore are not provided, even if demanded by a patient or family. For example, cardiopulmonary resuscitation may not be appropriate in a patient with progressive cardiogenic shock without a reversible underlying etiology. Fortunately, situations of medical futility, where members of the health care team disagree with the patient and/or family about whether therapies have an acceptable 7 likelihood of benefiting patient goals, are uncommon. Referral to a specialty palliative care or involvement of a hospital ethics committee should be considered for assistance when there are disagreements about potentially futile care. Deactivation of implantable cardioverter defibrillators in terminal illness and end of life care. Management of implantable cardioverter-defibrillators in hospice: a nationwide survey. Implantable cardioverter defibrillator deactivation: a hospice quality improvement initiative.
Lidocaine is often ineffective; amiodarone and procainamide appear to be superior order selegiline 5mg on-line. However order generic selegiline on line, in a randomized trial of out-of-hospital cardiac arrest purchase selegiline canada, neither amiodarone nor lidocaine 5 improved survival to hospital discharge. In general, an initial amiodarone loading dose of 15 mg/min is given during a 10-minute period. This dose is followed by an infusion of 1 mg/min for 6 hours and then a maintenance dose of 0. After conversion of the arrhythmia to a normal rhythm, it is essential to institute measures to prevent recurrence. In patients with symptomatic nonsustained tachycardia, beta blockers may prevent recurrences. Other drugs, such as sotalol, procainamide, mexiletine, and flecainide, may be required if amiodarone is not effective. Ventricular Arrhythmias in Patients with Cardiomyopathies See Chapters 61, 77, and 78. Septal alcohol ablation and myotomy/myectomy have been useful in reducing the outflow gradient, but their role in reducing ventricular arrhythmias has not been established. Mutations in genes that encode various proteins of the desmosome (plakoglobin, desmoplakin, plakophilin, desmoglein, and desmocollin) have been found to 12 cause the disease but are present in only approximately 50% of patients. Because most of the circuits and scarring are located on the epicardial surface, epicardial ablation is often required. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. Tetralogy of Fallot Chronic serious ventricular arrhythmias can occur in patients years after repair of tetralogy of Fallot (see Chapter 75). Replacement of the pulmonic valve and concomitant cryoablation of the outflow tract may be required to eliminate the tachycardia. Mutations in genes encoding proteins responsible for 18 intracellular calcium handling have been identified as causes of the disease. A family history of sudden death or stress-induced syncope is present in approximately 30% of cases. Left-sided or bilateral sympathectomy has been reported to be effective in a few cases (see Chapter 99). In addition, flecainide inhibits ryanodine receptor–mediated calcium release and has had some clinical 17 success. The U wave can also become prominent and merge with the T wave, but its role is not clear. The abnormal repolarization need not be present or at least prominent in all beats, but it may be apparent only on the beat before the onset of TdP (i. Long-short R-R cycle sequences usually precede the onset of TdP from acquired causes. In this recording the tachycardia spontaneously terminates, and a paced ventricular rhythm is restored. Motion artifact is noted at the end of the recording as the patient lost consciousness. Electrophysiologic Features The electrophysiologic mechanisms responsible for TdP are not completely understood. However, most data currently point to transmural reentry as the most likely mechanism of perpetuation. Isoproterenol, given cautiously because it may exacerbate the arrhythmia, can be used to increase the rate until pacing is instituted. The congenital form is a familial disorder that can be associated with sensorineural deafness (Jervell and Lange-Nielsen syndrome, autosomal recessive) or normal hearing (Romano-Ward syndrome, autosomal dominant). Sudden death can occur in this group of patients; it develops in approximately 10% of pediatric patients without preceding symptoms. Implantation of a permanent pacemaker to prevent the bradycardia or pauses that may predispose to the development of TdP may be indicated. Left-sided cervicothoracic sympathetic ganglionectomy that interrupts the stellate ganglion and the first three or four thoracic ganglia may be helpful and can be done thorascopically. The majority of evidence points to abnormalities in the transmural gradient of the action potential notch (caused by I ) present into the epicardium but not endocardium because of an abnormal transmural distribution of I (to see Chapter 35). BrS is more common in apparently healthy young Southeast Asians but also exists in other areas of the world and ethnicities. Placing the right precordial leads in the second or third intercostal1 3 space (“high leads”) can increase the sensitivity of detecting a type 1 pattern. According to these guidelines, a type 2 or 3 pattern is only diagnostic when it converts to a type 1 pattern with drug provocation. Drug challenge is not indicated in patients with spontaneous type 1 Brugada pattern (whether the patient is symptomatic or not) since there is no additional diagnostic value. Genetic testing may not be helpful in risk stratification, although it can be helpful in family screening if there is an identifiable causative mutation (see Chapter 33). In patients with diagnosed or suspected Brugada syndrome, fevers should be aggressively treated and drugs that can provoke Brugada syndrome should be avoided (see http://www. Early Repolarization Syndrome Most patients with early repolarization are not at risk for ventricular arrhythmias. This tachycardia is characterized by a left bundle branch block contour in lead V and an inferior axis. They probably provoke a compensatory sympathetic response because each is followed by a brief period of sinus tachycardia. The sinus pacemaker appears to be unstable because of the resultant changes in P wave morphology. In a small number of patients, the tachycardia seems to arise in the inflow tract or apex of the right ventricle. The tachycardias most often arise from the left posterior fascicle but can also arise (or exit) from the anterior fascicle. Entrainment has been demonstrated, which suggests reentry as a cause of some of the tachycardias. Anatomically, this area is an epicardial location near the junction of the middle cardiac vein and the coronary sinus. Although the mechanism and site of origin of this tachycardia have remained somewhat controversial, most evidence supports a ventricular origin. When the tachycardia is caused by digitalis, the extent of toxicity is frequently advanced, and the prognosis is poor. Electrophysiologically, bundle branch reentrant complexes are started after a critical S -H or S -H delay2 2 3 3. B, Delay in S -H and reversal of2 2 activation between His and right bundle during premature stimulation.
By F. Jorn. Rowan University.