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H. Bogir, M.B. B.A.O., M.B.B.Ch., Ph.D.

Deputy Director, Boston University School of Medicine

Parenteral infusions (intravenous or subcutaneous) of opioids can be self-administered by the patient using specially designed computerized pumps that can be set to deliver specific amounts of drug on demand or by continuous infusion. Sedation and drowsiness vary with the drug, the dosage, and the route of administration. Useful approaches to counteract the sedative effects include reducing the individual dose and prescribing it more frequently; using dextroamphetamine (2. Respiratory depression is the most serious adverse effect, but tolerance develops rapidly, allowing for prolonged use and dose escalation for chronic pain. In patients who are receiving chronic opioids for pain and who develop respiratory depression, diluted doses of naloxone (0. The occurrence of nausea and vomiting with one drug does not mean that all produce similar symptoms. Changing to a different opioid or using an antiemetic in combination can obviate this effect. Tolerance rapidly develops to the emetic effects of opioids so that after several days antiemetics often can be discontinued. Constipation should be prevented by providing a regular bowel regimen including cathartics, stool softeners, and careful attention to diet. The most common offender is meperidine because its active metabolic, normeperidine, accumulates and can cause seizures. Because the half-life of the normeperidine is 16 hours, it may take several days for toxic side effects to clear. Multifocal myoclonus occurs more commonly in patients with renal dysfunction receiving the meperidine. Such patients should be switched to alternative drugs such as fentanyl or methadone, which are not predominantly cleared by the kidney. Morphine has an active metabolite that accumulates in renal dysfunction and has been reported to play a role in its side effects. To prevent withdrawal, patients should be slowly tapered off their opioids; 25% of the total daily opioid dose prevents the development of abstinence symptoms. For reasons not well understood, the rate of tolerance development varies greatly among patients with pain. Increased opioid requirements are most commonly associated with disease progression rather than tolerance alone. With the development of tolerance, increases in the frequency or the dose of the opioid are required to provide continued pain relief. Because the analgesic effect is a logarithmic function of the dose of the opioid, doubling of the dose may be needed to restore full analgesia. There appears to be no limit to the development of tolerance; and with 108 appropriate dose adjustments, patients can continue to obtain pain relief. Cross-tolerance among the opioid analgesics is not complete, therefore, changing to an alternative opioid at a starting dose of one fourth to one half of the predicted equianalgesic dose may be advantageous. Tolerance is distinct from physical dependence, which is characterized by the appearance of withdrawal signs after drugs are abruptly discontinued, and from psychological dependence, which is epitomized by a concomitant behavioral pattern of drug abuse characterized by craving a drug for other than pain relief and overwhelming involvement in its procurement and use. From the available data based on studies on the chronic use of opioids in patients with cancer, few patients develop psychological dependence on the drug. This issue is controversial in management of patients with chronic non-malignant pain, but data indicate that such patients can be treated effectively with chronic opioid therapy. Guidelines for the use of chronic opioid therapy in non-malignant pain have been developed (Table 27-5). Some drugs increase the analgesic effects of the opioids, counteract their side effects, or act as analgesics themselves. Clear evidence suggests the analgesic efficacy of carbamazepine, baclofen, and pimozide in trigeminal neuralgia and of the tricyclic antidepressants in neuropathic pain. Similarly, several psychostimulants are effective in counteracting opioid-induced sedation (dextroamphetamine and methylphenidate) and in improving analgesia (dextroamphetamine and caffeine). For the other drugs in this group, anecdotal or survey data suggest their usefulness in various types of neuropathic pain (Table 27-6), and the physician must consider the risks and benefits of polypharmacy when trying to provide analgesia for patients with difficult and complex pain syndromes. This drug also has sedative and antiemetic properties again useful for severe pain in patients tolerant to opioid analgesics. For lancinating neuropathic pains, not only carbamazepine and phenytoin but valproate and gabapentin have been reported to be effective.

If atrial fibrillation must be treated on an urgent basis, for example, in a patient with the Wolff-Parkinson-White syndrome who has a very rapid ventricular rate and hemodynamic compromise, an initial shock of 200 J should be followed by 360-J shocks, as needed. Because the defibrillation energy requirement is a probability function and not a discrete value, subsequent shocks may be effective for cardioversion/defibrillation even when the first 360-J shock is ineffective. The risk of post-shock ventricular arrhythmias is increased in the presence of a supratherapeutic plasma concentration of digitalis, so cardioversion in the presence of digitalis toxicity should be avoided. Mild myocardial necrosis occasionally may occur if a total energy exceeding 425 J is delivered in a short period of time. Another rare complication of cardioversion is pulmonary edema, which may be due to transient left ventricular dysfunction. Post-shock bradycardia or asystole may occur because of vagal discharge or an underlying sick sinus syndrome. With the development of pulse generators small enough to implant in the infraclavicular area and endocardial leads that are inserted transvenously, the implantation procedure has been greatly simplified and now is very similar to that of permanent pacemakers. A single lead that contains a pacing-sensing electrode and two defibrillating coils can be used. If adequate defibrillation is not achieved with a single lead configuration, a subcutaneous patch electrode or subcutaneous array can be added. In another commonly used configuration, the pulse generator itself functions as an electrode, and a lead that has a pacing-sensing electrode at its tip and a distal defibrillating coil electrode is positioned at the right ventricular apex. Multiple other combinations of a chest wall patch electrode with defibrillating electrodes in the right ventricular apex, superior vena cava, or coronary sinus also can be used. Testing is performed at the time of implantation to determine the energy requirement for defibrillation. A safety margin of at least 10 J should be present; for example, if the maximum output of the pulse generator is 32 J, successful defibrillation should be achieved with shocks of 22 J or less in strength. Optimal programming is important for many reasons, including minimizing patient discomfort, reducing the chance of syncope with an arrhythmia episode, maximizing the battery life of the pulse generator, and preventing inappropriate shocks. Complications related to the implantation procedure include pneumothorax, myocardial perforation, and infection, all of which should have an incidence less than 1%. Complications associated with the subcutaneous or submuscular pocket into which the device is placed include hematoma formation and erosion of the pocket. A, In this patient, the stored electrogram demonstrates ventricular tachycardia, rate 300 beats per minute, indicating tht the shock was appropriate. He was treated with amiodarone to reduce the frequency of episodes of ventricular tachycardia. B, this patient received shocks because of paroxysmal supraventricular tachycardia at a rate of 206 beats per minute, which exceeded the programmed rate cut-off of 170 beats per minute. He underwent radiofrequency ablation of the paroxysmal supraventricular tachycardia and received no further inappropriate shocks. C, the stored electrograms in this patient indicate that the patient received inappropriate shocks that were triggered by atrial fibrillation, rate 180 beats per minute. This patient was trated with a beta-blocker to keep the ventricular rate less than 150 beats per minute during atrial fibrillation. Other lead complications include a fracture or insulation breakdown, either of which may result in a failure to defibrillate. However, urgent evaluation is necessary if the patient experiences flurries of discharges. Flurries of shocks may be triggered by atrial fibrillation with a rapid ventricular response, in which case aggressive management of the atrial fibrillation is indicated. In addition, flurries of shocks may be a manifestation of a lead fracture, in which case lead replacement is necessary. Radiofrequency energy is delivered through an electrode catheter whose tip is in contact with tissue that is critical to maintenance of the tachycardia. The radiofrequency energy results in resistive heating of the tissue and irreversible tissue destruction when the tissue temperature exceeds 50° C. Diagnostic electrophysiologic testing (see Chapter 50) and radiofrequency ablation often are performed during the same procedure, commonly on an outpatient basis. Depending on the type of tachycardia, sites in the heart are targeted for ablation based on the results of mapping (see Chapter 50) or as guided by specific anatomic landmarks.

Although heart failure patients with preserved systolic function are often considered to have diastolic dysfunction, there are many other explanations for this presentation, some of which are reversible or warrant specific therapy (Table 47-4). Ejection fraction measurements may be inaccurate, particularly when their technical quality is suboptimal. Regurgitant valve diseases may lead to a dissociation between the ejection fraction and underlying myocardial dysfunction, because in this setting the afterload may be very low. There are also a number of conditions in which left ventricular function is transiently impaired but subsequently measured ejection fractions may be normal; intermittent ischemia, presenting as episodic heart failure ("flash pulmonary edema") is the most important, because revascularization may be indicated. Severe hypertension with subsequent treatment and transient arrhythmias may also have temporary effects on ejection fraction. Some patients with alcoholic cardiomyopathy may exhibit very rapid recovery in ejection fraction when they cease drinking. The remaining patients most likely have diastolic dysfunction as the underlying disorder. Unfortunately, the non-invasive measurement of diastolic function remains problematic. The most common test used, Doppler echocardiography, is neither sensitive nor specific for diastolic dysfunction. Particularly in the elderly, Doppler mitral valve filling patterns show impaired early diastolic filling in the majority of subjects, whether or not they have evidence of heart failure. Thus, diastolic dysfunction is basically a diagnosis of exclusion based on accompanying conditions and circumstantial evidence. Many patients with chronic heart failure maintain a stable course and then abruptly present with acutely or subacutely worsening symptoms. Although this decompensation may reflect unrecognized gradual progression of the underlying disorder, a number of precipitating events must be considered and, if present, addressed (Table 47-5). An important focus is on changes in medications (by patient or physician), diet, or activity. Superimposed new or altered cardiovascular conditions, such as arrhythmias, ischemic events, hypertension, or valvular abnormalities, should be considered. Systemic processes such as fever, infection, or anemia may also cause cardiac decompensation. The symptoms generally reflect, but may be dissociated from, the hemodynamic derangements of elevated left- and right-sided pressures and impaired cardiac output or cardiac output reserve. Dyspnea, or perceived shortness of breath, is the most common symptom of patients with heart failure. The most important is pulmonary congestion with increased interstitial or intra-alveolar fluid, which activates juxtacapillary J receptors, which in turn stimulate a rapid and shallow pattern of breathing. Increased lung stiffness may enhance the work of breathing, leading to a perception of dyspnea. Central regulation of respiration may be disturbed in more severe heart failure, resulting in disordered sleep patterns and sleep apnea. Hypoxia, which is uncommon in heart failure patients unless there is accompanying pulmonary disease, suggests the presence of pulmonary edema. It should also be noted that dyspnea is a common symptom of patients with pulmonary disease, obesity, and anemia and in sedentary individuals. Orthopnea is dyspnea that is positional, occurring in the recumbent or semirecumbent position. It occurs due to the increase in venous return from the extremities and splanchnic circulation to central circulation with changes in posture, with resultant increases in pulmonary venous pressures and pulmonary capillary hydrostatic pressure. Nocturnal cough may be a manifestation of this process and is an underrecognized symptom of heart failure. Orthopnea is a relatively specific symptom of heart failure, although it may occur in patients with pulmonary disease who breathe more effectively in an upright posture and in individuals with significant abdominal obesity or ascites. However, most patients with mild or moderate heart failure do not experience orthopnea when they are adequately treated. Symptoms usually resolve over a period of 10 to 30 minutes after the patient arises, often gasping for fresh air from an open window.