Physicians have a specific responsibility toward patients who are hopelessly ill, dying, or in the end stages of an incurable disease. In a summary of current practices affecting the care of dying patients, we give particular emphasis to changes that have become commonplace since the early 1980s. Implementation of accepted policies has been deficient in certain areas, including the initiation of timely discussions with patients about dying, the solicitation and execution in advance of their directives for terminal care, the education of medical students and residents, and the formulation of institutional guidelines. The appropriate and, if necessary, aggressive use of pain-relieving substances is recommended, even when such use may result in shortened life. We emphasize the value of a sensitive approach to care--one that is adjusted continually to suit the changing needs of the patient as death approaches. Possible settings for death are reviewed, including the home, the hospital, the intensive care unit, and the nursing home. Finally, we consider the physician's response to the dying patient who is rational and desires suicide or euthanasia.
A byproduct of experience with the artificial kidney was the detection of reversible electrocardiographic "currents of injury" in patients with electrolyte imbalance. These changes occurred irrespective of anatomic alterations and resembled the changes of acute pericarditis or myocardial infarction. The electrolyte basis for the "current of injury" was established by the prompt abolition of the RS-T segment elevations, when the electrolyte imbalance was corrected by means of artificial hemodialysis.AREGULAR electrocardiographic feature of moderately advanced potassium intoxication is depression of the RS-T segments. The erroneous inference of myocardial infarction is generally avoided because of the direction of the RS-T shifts, the clinical setting in which this phenomenon is recorded and its association with other electrocardiographic abnormalities distinctive of potassium intoxication. In a few exceptional instances of potassium intoxication, however, elevation rather than depression of the RS-T segments may be produced. toxication. He gave no history of chest pain or compression. On examination the heart rate was 150, the cervical veins were distended, coarse bubbling rales were heard throughout the lung fields, a gallop rhythm was heard at the cardiac apex and the liver edge was felt two fingerbreadths below the right costal margin. Tracings recorded on the afternoon of admission showed sinus tachycardia ( fig. 1 B), with left bundle branch block. The RS-T segments in leads V,, V2 and lead aVR showed rather pronounced elevation, probably more than could be accounted for purely on the basis of left bundle branch block. Later in the afternoon the heart rate was 108 and the cardiac rhythm irregular and disturbed by runs of probable paroxysmal ventricular tachycardia. Over the right precordium the RS-T segment elevation was now more pronounced and associated with deep broad Q waves ( fig. 1 C). The persistence of these changes was regarded as strong evidence for a "current of injury" and, it was believed, could not be attributed to left bundle branch block. At 6:40 p.m. hemodialysis was begun. At this time the serum potassium level was 7.8 mEq. per liter, sodium 127 mEq. per liter and the carbon dioxide content 9 mM per liter. Because the patient had marked pulmonary edema, the concentration of sodium in the bath fluid of the artificial kidney was maintained at 127 in order to avoid sodium loading in the presence of heart failure. The bath potassium concentration was initially set at 2 mEq. per liter but following the development of arrhythmia, was raised to 5. Two hours after the beginning of dialysis when the serum potassium level had fallen to 2.6 mEq. per liter and the sodium level had remained at 128 mEq. per liter, the electrocardiogram showed striking improvement. A supraventricular tachycardia (ventricular rate 210) had developed, the QRS complex had sharpened and shortened and the RS-T segment shifts over the right ventricle had almost disappeared ( fig. 1 D). Though the patient improved temporarily af...
Graham Steell (1888) first described a variable and at times indistinct diastolic murmur over and slightly below the pulmonary area: this he attributed to "pulmonary regurgitation ... occurring independently of disease or deformity of the valves, and as the result of long-continued excess of blood pressure in the pulmonary artery." He later (1895) reported 60 cases of mitral stenosis and considered that only one had the murmur of "high pressure" in the pulmonary artery. Kezdi et al. (1955) reviewed 95 cases of mitral stenosis and found only one that they considered had the functional murmur of pulmonary regurgitation. This incidence of pulmonary regurgitation is low and reflects the strict criteria that were applied in order to arrive at a certain diagnosis.In this department consideration of the diagnosis of pulmonary regurgitation seemed to arise more frequently, and there was often disagreement among observers about patients with early basal diastolic murmurs. This arose partly because some of these murmurs were soft and transient and partly because there was often little supporting evidence to distinguish pulmonary from aortic regurgitation. The question particularly came up in patients with rheumatic heart disease. For these reasons an attempt was made to demonstrate pulmonary regurgitation by a dye method in 9 patients undergoing cardiac catheterization. MATERIAL AND METHODThe nine patients investigated fell into three groups: Group A, three patients who were catheterized for routine purposes and were not thought to have a Graham Steell murmur; Group B, four patients in whom the presence of a Graham Steell murmur was debatable; and Group C, two patients in whom a Graham Steell murmur was clinically agreed to be present. The diagnosis of a Graham Steell murmur was made clinically on the basis of a blowing early diastolic murmur heard in the left 2nd and 3rd intercostal space in the absence of peripheral signs of aortic regurgitation and in the presence of a strong systolic pulsation over the area of the right ventricle, a palpable pulmonary artery impulse, an accentuated second sound in the pulmonary area, X-ray signs of pulmonary artery enlargement, and electrocardiographic evidence of right ventricular hypertrophy.At right heart catheterization a number 8 catheter was placed 1-2 cm. distal to the pulmonary valve, and a number 9 catheter with multiple perforations at the end (Goodale-Lubin tip) was placed in the right ventricle just below the pulmonary valve. In the first three studies (patients B4, B5, and B6), 2 ml. of Evans blue (T-1824) were injected into the pulmonary artery in less than 1 second, and at the same instant fractional collection of blood from the right ventricle was begun with a Cornwall double valved syringe at a rate of 2 ml. per second. This had the disadvantage that, with a single bolus of dye rapidly injected into the pulmonary artery, streaming from the tip of the catheter was great and regurgitant dye that appeared transiently might be missed with the interrupted method of samplin...
Clinical experience suggests that the administration of cortisone may reactivate an apparently healed tuberculous infection in man (
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.