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Biomedical subjects

J Rabson

Publications and source records attributed to J Rabson.

8 recordsLinked to original sources
PubMed1984

Use of sodium bicarbonate to treat tricyclic antidepressant-induced arrhythmias in a patient with alkalosis.

Sodium bicarbonate has been recommended for the treatment of arrhythmias induced by tricyclic antidepressants. It is unclear, however, whether this therapy is effective only in the presence of acidosis. A case is presented in which there was an immediate response to sodium bicarbonate in three episodes of ventricular tachycardia despite the presence of alkalosis on two of the three occasions. Given the poor response to conventional therapy of arrhythmias induced by tricyclic antidepressants the use of sodium bicarbonate may be reasonable even in the presence of alkalosis. However, in the presence of pre-existing respiratory or metabolic alkalosis, such therapy is not without risk, and it is suggested that it be reserved for life-threatening situations when the arrhythmia has failed to respond to hyperventilation or antiarrhythmics or both.

Adult↗
PubMed1984

Clinical effectiveness of the Du Pont aca measurement of creatine kinase MB in serum from patients in a coronary-care unit.

We evaluated the clinical effectiveness of measuring creatine kinase (CK; EC 2.7.3.2) isoenzyme MB and lactate dehydrogenase (LD; EC 1.1.1.27) isoenzymes in diagnosis of acute myocardial infarction. We used an agarose electrophoresis method to measure CK and LD isoenzymes and the Du Pont aca column method to measure CK-MB. Serial blood specimens were drawn from 100 patients consecutively admitted to our Coronary Care Unit. Because of the low diagnostic specificity for CK-MB measurements by both agarose electrophoresis and the discrete-analysis method, as compared with reported values, we re-evaluated our isoenzyme data by using Receiver Operating Characteristic curves. Such analysis of the data established optimal decision levels of greater than or equal to 25 U/L and greater than or equal to 18 U/L plus greater than or equal to 6% of total CK for serum CK-MB measured by the agarose electrophoresis and the aca methods, respectively, and an optimal decision level of greater than or equal to 0.92 for the ratio of LD 1/2 measured after agarose electrophoresis. At these decision levels we obtained a sensitivity of 100%, 100%, and 95% and a specificity of 94%, 92%, and 90% for CK-MB (agarose electrophoresis), CK-MB (aca), and the LD 1/2 ratio, respectively.

Autoanalysis↗
PubMed1983

Dopamine, dobutamine, and phentolamine effects on pulmonary vascular mechanics.

The pressure-flow (P-Q) relationship of the pulmonary vasculature, in an isolated canine lobe perfused under classical zone II conditions, can be characterized by a rectilinear segment at high flow, a curvilinear segment at low flow, and a pulmonary arterial pressure (Ppa) that exceeds alveolar pressure at zero flow. This demonstrates the presence of critical closure in the pulmonary vascular bed. Effects of drugs on pulmonary vascular resistance (PVR) must take the normal P-Q relationship into account. We examined the effect of dopamine (D) and dobutamine (DB), alone and in combination with phentolamine (P), on the slope of the rectilinear segment of the P-Q curve (equivalent to vascular conductance), the extrapolated Ppa intercept (Ppai), and the Ppa at zero flow (Ppaz). Low-dose D (0.4-0.8 mg) and DB (1.0-5.0 mg) did not significantly alter any parameter from control. Higher-dose D (1.2-6.8 mg) and DB (13-38 mg) decreased vascular conductance 32.3 +/- 12.1 (SE) to 50.45 +/- 5.6% (P less than 0.05), and P alone increased conductance 12.0 +/- 2.6% (P less than 0.01) from control with no significant effect on Ppai or Ppaz. The change in conductance with D and DB alone was abolished when either drug was given in combination with P. Ppaz and Ppai decreased significantly from control with DB in combination with P when no significant effect on vascular conductance was noted. The results suggest that lung vessels determining changes in flow resistance are pharmacologically distinct from those subserving critical closure in the pulmonary vascular bed.

Animals↗
PubMed1983

Hemodynamic mechanisms in anaphylaxis.

Intravenous administration of ascaris suum antigen (1 mg) as well as histamine (5 mg) was associated with rapid and marked reductions in cardiac output (QT) and systemic arterial pressure (Pa) in anesthetized mechanically ventilated dogs. When venous return was maintained constant by an external pump reservoir system, both antigen and histamine caused rapid reductions in the reservoir blood volume consistent with peripheral pooling. In addition, interruption of the splanchnic arterial inflow by occlusion of the descending thoracic aorta restored the cardiac output to control during histamine shock, whereas QT during antigen shock was unaffected by aortic occlusion, even though the circulatory failure was of similar magnitude. Therefore, we conclude that differences in responses of antigen and histamine shock to aortic occlusion indicate that mechanisms leading to peripheral pooling of blood are different with the two agents. In addition, stability of left atrial pressure following the administration of either agent, when the venous return is maintained constant, suggests that intrinsic myocardial dysfunction is not a major initiating mechanism in the two shock states studied.

Anaphylaxis↗
PubMed1982

Critical closure in the canine pulmonary vasculature.

The vascular pressure-flow (P-Q) relationships in zone II (West et al.) were studied in isolated canine left lower lobes, in order to characterize the total resistance in the pulmonary vascular bed with respect to incremental or flow resistance and critical closure. At each of five levels of static lung inflation, the P-Q relationship was curvilinear at low flow and rectilinear at higher flows. The slope of the linear portion was not significantly different at alveolar pressures (PA) = 5, 7, or 9 cm H2O, but decreased significantly at PA = 11 and 15 cm H2O ((P less than 0.05), indicating an increase in flow resistance. The pulmonary artery pressure (Ppa) fell to the same value at zero flow regardless of inflation level [10.1 +/- 1.0 (SD) cm H2O at PA = 5 cm H2O to 10.9 +/- 2.7 (SD) at PA = 15 cm H2O]. The Ppa intercept (Ppai), extrapolated from the linear portion of the P-Q curve and representing the average closing pressure for the vascular bed, increased from 16.0 +/- 1.8 (SD) cm H2O at PA = 5.0 to 26.5 +/- 4.4 (SD) cm H2O at PA = 15 (P less than 0.05) in a direct one-to-one relationship with the increase in PA. Since this results in a constant transmural gradient at the alveolar vessel level, these vessels must be the major fraction which undergo critical closure. Operationally defined vascular compliance, determined from the slope of a simultaneously obtained pressure-volume (P-V) curve, decreased significantly from 1.51 +/- 0.62 (SD) ml/cm H2O at PA = 5.0 H2O to 0.87 +/- 0.27 ml/cm H2O at PA = 15 cm H2O (P less than 0.05).

Animals↗
PubMed1979

Left ventricular hemodynamics during respiration.

We have investigated the mechanisms involved in the inspiratory fall in left ventricular stroke volume (LVSV), utilizing a spontaneously breathing dog on right-heart bypass (RHBP). We have been able to control lung volume, pulmonary artery inflow, and right-heart volume (RHV). During Mueller maneuvers in one series, RHV was allowed to increase as pleural pressure (Ppl) fell; in a second series, changes in RHV were excluded. In both series LVSV fell significantly, associated with a significant rise in the transmural (relative to Ppl) aortic diastolic pressure, reflecting an increase in the effective LV afterload. The transmural left ventricular filling pressure did not fall, a fact inconsistent with decreased pulmonary venous return, causing the fall in LVSV. The LVSV fell significantly more when RHV was allowed to increase as when it was held constant with all other variables showing no statistical change. Thus, increases in both RHV and effective LV afterload are created by the inspiratory fall in Ppl and summate to decrease LVSV.

Airway Obstruction↗
PubMed1978

Effects of respiration on cardiac performance.

The conventional explanation for the fall in left ventricular stroke volume (LVSV) with inspiration is that blood pools in the lungs, thereby decreasing pulmonary venous return. In anesthetized dogs, we have found an increase in left ventricular filling pressure (LVFP) with both constant and increasing lung volume during an inspiratory effort. Transmural aortic diastolic pressure rises as LVSV falls and LVFP rises consistent with the hypothesis that a fall in pleural pressure afterloads the left ventricle. Additionally the increase found in right ventricular filling pressure with inspiration may adversely affect LV performance by decreasing LV compliance and/or contractility. Our findings are incompatible with pooling of blood in the lungs being the primary determinant of the fall in LVSV with inspiration.

Animals↗