The effects of DRGs on the pattern of admission of medicare patients.
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Biomedical subjects
Publications and source records attributed to D Garner.
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Clinically, asystole or a bradyarrhythmia may follow countershock of ventricular fibrillation (VF) in up to 40% of attempts. This study evaluated the effects of artificial cardiac pacing, calcium chloride (CaCl2), and epinephrine in postcountershock asystole/bradycardia. Micromanometer catheters were positioned in the aorta (Ao) and right atrium (RA) of ten dogs and VF induced by right ventricular (RV) stimulation. After 2 min of VF, a 400-J countershock was given. In six animals, asystole or a pulseless bradyarrhythmia followed one countershock. In four animals, up to three countershocks were needed to terminate VF and resulted in asystole or a pulseless bradyarrhythmia. Thirty seconds after termination of VF, cardiac pacing was begun in all animals using conventional RV endocardial pacing (RVEP) or a transcutaneous transthoracic pacing (TTP) technique. RVEP and TTP produced ventricular depolarizations, but electrical capture was never associated with Ao pressure fluctuations. After 2 min of pacing, CaCl2 was given and chest compressions and artificial ventilations (CPR) initiated. CaCl2 had no effect on CPR pressures. After 2 min of CPR, RVEP and TTP were again studied; capture without Ao pressure fluctuations was seen in all animals. Epinephrine was then given and CPR reinstituted. Epinephrine produced a significant increase in CPR Ao systolic pressure (58 +/- 13 to 84 +/- 24 mm Hg, p less than .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 +/- 4 to 34 +/- 8 mm Hg, p less than .001). Within 94 +/- 53 sec after epinephrine, spontaneous circulation was restored in eight animals.(ABSTRACT TRUNCATED AT 250 WORDS)
The Vascular-Access-Port (VAP) is a subcutaneous implantable device designed for repeated venous blood sampling in humans. With slight modifications the device has been used in the arterial and venous systems of dogs. This device allows for chronic repeated arterial blood pressure monitoring, monitoring of cardiac outputs, and blood sampling in conscious dogs. Infection, vascular thrombosis, and catheter extraction have not occurred. This modified VAP has been used for 6 mo and in 25 dogs to date without any failure to determine arterial blood pressure and cardiac output.
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Out-of-hospital therapy for cardiac arrest due to bradyarrhythmias or asystole is pharmacologic and the outcome is uniformly dismal. Optimal therapy for the latter disturbances may be artificial cardiac pacing, but conventional invasive pacing techniques are not employed or are of limited value in the out-of-hospital and emergency department setting. This investigation compared the hemodynamic effects of two techniques of non-invasive external pacing: 1) transcutaneous transthoracic pacing (TTP) and 2) tongue-to-epigastrium pacing (TEP), with conventional transvenous right ventricular endocardial pacing (RVEP) in a closed-chest, chronic heart block canine model. All techniques significantly increased (p less than .001) cardiac output (CO). However, CO and mean arterial pressure (MAP) measured during external pacing with either non-invasive technique were significantly greater than that during RVEP (p less than .001). TEP produced vigorous skeletal muscle stimulation and, in the canine model, it produced contraction resulting in impaired ventilation, hypoxemia, and a decrease in systemic vascular resistance. TTP in this model resulted in improved MAP and CO when compared with control and RVEP values and did not affect arterial or mixed venous blood gas values. Thus, this study demonstrates that noninvasive TTP is comparable to RVEP in its hemodynamic effects. TTP may offer definitive non-invasive therapy for a subset of victims of out-of-hospital cardiac arrest.
The effect of epinephrine on glucose homeostasis has been studied extensively in many species, but there is little data on the effects of another catecholamine, norepinephrine. This study was designed to examine the alterations that occur in insulin and glucagon secretion during a chronic low-dose infusion of norepinephrine in free-roaming dogs. A total of four intravenous glucose tolerance tests and insulin-induced hypoglycemia tests were performed on each of five dogs infused with norepinephrine (1.4 g/min) for 3 mo and on each of eight control dogs. The infusion resulted in a threefold increase in plasma norepinephrine without a significant effect on blood pressure. Fasting serum glucose was elevated significantly in the norepinephrine-infused dogs [102.4 +/- 2.1 vs. 92.8 +/- 1.7 (SE) mg/100 ml]. Fasting plasma glucagon was elevated by the norepinephrine infusion (58.4 +/- 7.6 vs. 31.3 +/- 3.1 pg/ml), whereas fasting serum insulin was inhibited (12.3 +/- 1.3 vs 16.8 +/- 1.7 U/ml). Glucagon secretion in response to hypoglycemia was markedly enhanced in the infused dogs compared with controls. It has been reported that the infusion of norepinephrine in humans will inhibit insulin secretion and increase serum glucose concentrations but have no effect on serum glucagon concentrations. The stimulation of glucagon by norepinephrine has been demonstrated in the isolated, perfused canine pancreas but has not been reported previously in the free-roaming dog.
Norepinephrine, a known inducer of myocardial hypertrophy, was found to have marked effects on the myocardial adrenergic system, which occurred prior to the development of a significant increase in heart weight. The chronic subhypertensive infusion (1.4 microgram/min) in free-roaming dogs produced a threefold increase in plasma norepinephrine (determined by radioimmunoassay). After 3 mo of infusion, right and left ventricular norepinephrine content (ng/mg protein) decreased significantly by twofold (right, 2.50 +/- 0.24; left, 2.08 +/- 0.36) compared with controls (right, 4.76 +/- 1.48; left, 4.65 +/- 1.49), and beta-receptor density (125I-pindolol) increased (right, 0.122 +/- 0.029; left, 0.153 +/- 0.021) over the controls (right, 0.082 +/- 0.015; left, 0.069 +/- 0.008 pmol/mg protein). Accompanying the beta-receptor changes, isoproterenol-stimulated adenylate cyclase activity also increased significantly [right, 29.2 +/- 2.1; left, 29.5 +/- 1.0 vs. controls, right, 13.8 +/- 1.1; left, 20.2 +/- 2.2 pmol adenosine 3',5'-cyclic monophosphate (cAMP) generated X min-1 X mg protein-1]. Because the above changes occurred in the absence of cardiac hypertrophy, it suggests that alterations in the myocardial adrenergic system are dependent on the stimulus (in this case norepinephrine) invoking the change and not the degree of hypertrophy. It also suggests that changes in the adrenergic system may not directly reflect the mechanism involved in the development of hypertrophy.
Norepinephrine infusion in dogs has been shown to cause ventricular septal hypertrophy that mimics the syndrome of hypertrophic cardiomyopathy in humans. To characterize the mechanisms involved in septal hypertrophy, the adrenergic system of the right and left ventricles and the septum were analyzed before and after norepinephrine infusion. In the normal unperturbed state, the septum was found to be more sensitive to beta-adrenergic stimulation than either the right or left ventricles. That is, more cyclic AMP could be generated with a smaller dose of beta-agonist (isoproterenol) in septal tissue homogenate than in homogenates of the right or left ventricles. With infusions of norepinephrine (1.4 micrograms/min) to subhypertensive levels over 3 months, beta-receptor number increased twofold to threefold in the ventricles and septum. Adenylate cyclase activity also increased in the ventricles, but not in the septum. The sensitivity of adenylate cyclase to beta-agonist stimulation increased in the septum but remained unchanged in the right and left ventricles. We conclude that the alterations in the myocardial adrenergic system occur in response to the norepinephrine infusion and are not a consequence of hypertrophy. We formulated a hypothesis suggesting that depleted tissue stores of cyclic AMP and/or adenosine triphosphate may be one of the mechanisms involved in the development of hypertrophic cardiomyopathy.
Ventriculographically derived ejection fraction (EF-V) is the most frequently used method to measure left ventricular (LV) function, However, significant error may result in the measurement of end-systolic volume (ESV), which is used to calculate EF-V. This error is ascribed to the variable, irregular, nonellipsoidal geometry of the end-systolic ventricular chamber. Since stroke volume (SV) is determined more accurately by dilution methods than by ventriculography, an improved measure of ESV can be calculated by subtracting green dye determined SV from the ventriculographic determined end-diastolic volume (EDV). The purpose of this study was to measure a correlated ejection fraction (EF-C) using EDV by ventriculography and SV derived using green dye. In eight anesthesized dogs cardiac outputs (COs) were calculated by green dye and left ventriculography. CO determined by ventriculography was greater than that measured by green dye (p less than 0.005). EF-V (55 +/- 15%) was always greater than EF-C (32 +/- 12%) (p less than 0.005). These studies (1) may partially explain the discrepancy in CO calculated from the use of dilution methods and ventriculography and (2) present a method to improve the calculation of LV ejection fraction.
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Five mongrel dogs with chronically implanted catheters in the left atrium, mid-thoracic aorta, and right atrium were continuously infused with subhypertensive doses of norepinephrine for 3 months. Left ventricular cineangiography, determinations of aortic pressure, and cardiac output were performed in the conscious dog. After 3 months of continuous norepinephrine infusion, stroke volume increased from 38 +/- 3.0 to 67 +/- 8.0 ml. (p less than .01), the left ventricular end-diastolic volume increased from 72 +/- 6.4 to 89 +/- 12.9 ml. (p less than .05), and the ejection fraction increased from 52 +/- 3.6 to 76 +/- 3.6% (p less than .005). We postulate that norepinephrine results in an increased myocardial function by producing physiological myocardial hypertrophy.
A chronically and transseptally implanted left atrial catheter was utilized to perform repeated cineangiography in the conscious dog. The advantage of this preparation is that catheter placement does not require a thoracotomy. Left ventricular function was compared in the same pentobarbital-anesthetized and conscious dog. Anesthesia significantly depressed myocardial function as was demonstrated by a decrease in ejection fraction and segmental circumferential fiber shortening velocity (VCF) and an increase in end-diastolic volume. In addition, no difference in Vcf occurred between the base and the apex. Since anesthesia produced regional difference in the degree of depression of VCF, we conclude that anesthesia will produce patterns of ventricular contraction which are variable and unpredictable. Consequently, we recommend the use of the conscious dog and this preparation in order to evaluate myocardial function.
Human alpha-1-antichymotrypsin has been purified to homogeneity by the following sequential steps--(a) ammonium sulfate fractionation; (b) chromatography on Cibacron Blue Sepharose at pH 7.0; and (c) chromatography on SP-Sephadex C-50 at pH 5.5. The inhibitor has a molecular weight near 68,000 and contains approximately 26% carbohydrate alpha-1-Antichymotrypsin has an amino-terminal arginine and a carboxy-terminal glycine. It also has some homology with alpha-1-PI based on amino-terminal sequence analysis of both proteins. Complexes of alpha-1-antichymotrypsin with human chymotrypsin and human leukocyte cathepsin G are stable in sodium dodecyl sulfate and have molecular weights near 90,000 suggesting 1:1 complex formation on a molar basis between inhibitor and enzyme.
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Previous methods of internal calibration for cineangiography have made use of reference objects such as catheters or wires of known length or diameter. Such devices have either insufficient X-ray resolution, or require a specific orientation within the ventricle which is difficult to confirm. External calibration methods, while eliminating these errors, can only estimate actual position of the left ventricle. The use of a Swan-Ganz balloon catheter as a calibration object diminishes these problems. When positioned within the left ventrical and filled with a radiopaque medium, the balloon is of sufficient size and density to avoid errors induced by previously employed objects. The inflated balloon geometry is simple and reproducible. The use of this internal calibration catheter markedly diminishes major sources of errors in the determination of ventriculograms for both dogs and humans.
A method is described for obtaining left and right ventricular endocardial biopsies repeatedly over a period of 3-6 mo in the dog. The left ventricular endocardial biopsy technique consists of the placement of a catheter via the venous route across the atrial septum and into the left ventricle. The biopsy catheter is in turn placed within this transseptal catheter. Tissues obtained by this method were satisfactory for both light and electron microscopic examination. At postmortem examination, only minimal and insignificant damage existed at the biopsy site. Consequently, we recommend this technique for the study of progressive pathologic changes in the endocardium that occur during the course of an experiment which can be identified and quantified in comparison to the control state.
A preparation for performance of renal clearances in the conscious dog is described. The important aspect of the technique is the use of a Pavlov sling and a specially designed restraining apparatus. Of most importance is the use of a 7 French Swan-Ganz balloon-tipped catheter for urinary bladder catheterization. The use of male dogs obviated the need for an episiotomy. No special training of the animals was required. The animals tolerated long-term and repeated catheterization without any evidence of infection or trauma.
A method is presented for a relatively simple nontraumatic chronic left heart catheter preparation for the study of left ventricular hemodynamics in the conscious dog. In 30 dogs an 8 Fr Cordis catheter was modified and implanted into the left ventricle via the right atrial septum. Transseptal catheterization was performed without significant morbidity and mortality. Left ventricular cineangiograms and pressures and cardiac outputs have been repeatedly performed on fully conscious dogs with no apparent discomfort displayed by the dog.