Effect of afterload reduction on plasma volume during acute heart failure

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.     

Modifiable Failures in the Colorectal Cancer Screening Process and Their Association With Risk of Death

1. Download high-res image (240KB)
2. Download full-size image

     

Radionuclide analysis of peak filling rate, filling fraction, and time to peak filling rate. Response to supine bicycle exercise in normal subjects and patients with coronary disease

Using gated equilibrium radionuclide angiography, variables of diastolic filling were analyzed at rest and during supine bicycle exercise in normal subjects (Group 1, n = 18), coronary patients with normal resting ejection fractions (Group 2, n = 26), and coronary patients with reduced resting ejection fractions (Group 3, n = 8). Indexes analyzed were peak filling rate and filling fraction during the first third of diastole. At rest, the peak filling rate was significantly lower in coronary patients than in normal subjects (3.18 +/- 0.82 end-diastolic volume [EDV]/s in Group 1 versus 2.41 +/- 0.66 EDV/s in Group 2, p less than 0.005; and 1.34 +/- 0.26 EDV/s in Group 3, p less than 0.001 versus Group 1). These differences persisted at peak exercise. Coronary patients also had significantly lower filling fractions at rest and during exercise than did normal control subjects. The time from end-systole to peak filling rate was longer at rest in patients in Group 2 (203 +/- 52 ms) than in subjects in Group 1 (172 +/- 50 ms, p less than 0.025). This remained true when the time to peak filling was normalized by the R-R interval. Although the exercise time to peak filling was longer in coronary patients in both Groups 2 and 3 than in Group 1, these differences were not apparent when the interval was normalized by the R-R interval. Thus, abnormalities in peak filling rate and filling fraction exist in patients with coronary disease both at rest and during exercise, but large overlaps exist between normal and coronary patients. Caution is advised in comparing the timing of events during diastole because apparent group differences may be related in part to rest or exercise heart rate.     

Sensitivity and specificity of nuclear phase analysis versus ejection fraction in coronary artery disease

Phase standard deviation (SD) and skew characteristics of the first Fourier harmonic of equilibrium radionuclide volume curves were examined and compared during rest and during supine bicycle exercise with ejection fraction (EF) changes and the development of ischemia in 17 control subjects and in 2 groups of patients (n = 57) with coronary artery disease (CAD). Group I comprised 37 patients with CAD; IA was a subgroup of 20 patients with previous myocardial infarction (MI) and IB a subgroup of 17 patients with CAD without MI (all with coronary stenosis greater than 75% diameter narrowing). Group II comprised 20 patients with CAD who had undergone coronary bypass surgery. In the Group I subjects, phase SD was the most sensitive indicator of CAD at rest (Group I, 56%; Group IA, 70%, and Group IB, 29%), and the EF was the most sensitive indicator at submaximal (Group I, 78%; Group IA, 86%, and Group IB, 64%) and maximal exercise (Group I, 70%; Group IA, 93%, and Group IB, 53%). When phase SD and skewness were combined with EF changes, little increase in sensitivity occurred in Group I (rest 61%, submaximal exercise 88% and maximal exercise 76%). The results from Group II subgroups were qualitatively similar to those observed with Group I subgroups. These data reveal a marginally improved sensitivity for detection of CAD during supine bicycle radionuclide ventriculography when phase measurements were added to changes in global EF values.     

Constrictive pericarditis after myocardial revascularization: report of three cases.

Although postoperative constrictive pericarditis is rare, the diagnosis should be considered when unexplained right-sided heart failure develops after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.     

Investigation of insulin resistance during diabetic ketoacidosis: role of counterregulatory substances and effect of insulin therapy.

It has been generally accepted that insulin resistance (IR) exists in diabetic subjects during episodes of ketoacidosis (DKA). However, little experimental data exist regarding this question. We have studied IR in nine untreated diabetic subjects (mean age 20 yr) both during their initial episode of DKA and after 2–7 wk of insulin therapy. The experimental protocol consisted of a 150-min intravenous infusion of glucose (6 mg/kg/min) and insulin (80 mU/min). Under these conditions steady-state plasma glucose (SSPG) and insulin (SSPI) levels were reached by 90 min and maintained for the duration of the study. Since all subjects achieved similar SSPI and all received the same glucose load, the SSPG could be used as a measure of an individual's IR. In addition, steady-state plasma levels of glucagon, cortisol, growth hormone, and free fatty acids were measured in an attempt to gain insight into their roles in the maintenance of IR during DKA. Although mean (± SE) SSPI levels were the same during both study periods (93 ± 4 versus 92 ± 4 μU/ml), there was a marked difference between the initial and posttherapy SSPG levels for the nine subjects 342 ± 32 versus 104 ± 16 mg/100 ml,p < .001). Mean steady-state plasma levels of growth hormone, corticol, and free fatty acids were significantly higher during the initial studies, but only cortisol and free fatty acid levels correlated significantly with their corresponding SSPG levels. Steady-state plasma glucagon levels were the same during both study periods, and individual levels did not correlate with associated SSPG levels. These studies demonstrate that significant IR was present in these subjects during DKA as compared to the posttherapy period. Furthermore, the results suggest that while increased plasma concentrations of cortisol and free fatty acids may be involved in the maintenance of IR during DKA, elevated levels of plasma growth hormone and glucagon are not necessary for this phenomenon.     

Intravenous and oral prenalterol in congestive heart failure. Effects on systemic and coronary hemodynamics and myocardial catecholamine balance

Systemic and coronary hemodynamic effects of prenalterol, a beta-1 receptor agonist, were determined in patients with chronic congestive heart failure, initially after intravenous administration (10 patients) and then after oral administration (eight patients). Cardiac index increased by 33 percent and 30 percent after intravenous and oral prenalterol, respectively. The increase in stroke volume index and stroke work index and decrease in pulmonary capillary wedge pressure and systemic vascular resistance were not significant. Myocardial oxygen consumption and coronary sinus blood flow increased in the majority of patients, although these changes were not statistically significant. There were no significant changes in transmyocardial norepinephrine or epinephrine balance. The systemic and coronary hemodynamic effects of both intravenous and oral prenalterol were similar. Major side effects included sudden death (two patients) and hypotension and bradycardia (three patients) during oral prenalterol treatment. It is concluded that improved left ventricular function following both intravenous and oral prenalterol may be associated with increased myocardial oxygen consumption, and serious adverse effects may occur during prenalterol therapy.     

Mustard operation in the 1st month of life

Since April 1976, nine infants less than 1 month of age underwent a Mustard intraatrial baffle procedure. All had transposition of the great arteries and were persistently symptomatic or hypoxic after the Rashkind balloon atrioseptostomy. Two had an associated large ventricular septal defect patched at the time of physiologic correction. The average age of the infants was 11.6 days (range 36 hours to 28 days). Weight averaged 3.4 kg (range 2.5 to 4.2). In all the Mustard procedure was performed using deep hypothermie circulatory arrest, averaging 71 minutes (range 48 to 88) at a mean core temperature of 13 °C. An average of 2.8 days of postoperative ventilatory assistance was required. One death occurred in a 28 day old male infant with an associated ventricular septal defect who, the morning after operation, had a sudden unresponsive cardiac standstill. The postoperative hospitalization period averaged 15 days (range 10 to 23). Follow-up evaluation has extended from 4 to 63 months (average 31). Six patients were restudied 2 to 21 months postoperatively. One had obstruction of the superior limb of the baffle, which had separated from the right atrial wall permitting a modest right to left shunt. She has had uneventful repair employing a unique modification of Senning's operation. Another child has asymptomatic partial obstruction of the superior limb of the baffle demonstrated angiographically. None has pulmonary venous obstruction and all have prevailing normal sinus rhythm. Significant right ventricular dysfunction has been demonstrated in one. Early correction in these persistently symptomatic or hypoxic neonates with transposition of the great arteries with or without a ventricular septal defect has obviated the need for palliative operations and produced gratifying early and late results.     

Specific binding of 1,25 dihydroxyvitamin D3 in lymphocytes

We examined ten cellular or tissue sources of lymphocytes for specific binding of 1,25(OH)₂D₃, the hormonally active form of vitamin D₃. A specific-binding protein was found in three of these sources. Scatchard analysis of cytosol from a follicular lymphoma cell line revealed binding sites with a Kd of 7.0 × 10^?11 and a receptor concentration of 6.6 fmol/mg protein. Sucrose density centrifugation of ³H-1,25(OH)₂D₃ labeled cytosol showed a 3.75 peak which was absent in cytosols incubated with excess nonradioactive 1,25(OH)₂D₃. The relative amounts of vitamin D₃ metabolites required to displace 50% of the specifically bound ³H-1,25(OH)₂D₃ were 1,25(OH)₂D₃: 1,24,25(OH)₃D₃: 25(OH)D₃: 24,25(OH)₂D₃ = 1: 180: 1000: 2700. Excess vitamin D₃, cortisol, and estradiol failed to displace ³H-1,25(OH)₂D₃. Scatchard analysis of spleen cytosol from a patient with prolymphocytic transformation of chronic lymphocytic leukemia demonstrated a binding protein with a Kd of 1.2 × 10^?10 and a receptor concentration of 0.2 fmol/mg protein. DNA cellulose binding confirmed the presence of the specific-binding protein in this cytosol. Specific binding of ³H-1,25(OH)₂D₃ was also quantitated in a cell line from a patient with Burkitt's lymphoma with a Kd of 0.3 × 10^?10 and a receptor concentration of 29.6 fmol/mg protein. No specific binding of ³H-1,25(OH)₂D₃ was observed in lymphocytes from seven other malignant and nonmalignant sources. These results are the first to demonstrate a specific-binding protein for 1,25(OH₂D₃ in lymphocytes from tissue and from these specific cell lines. The presence of this protein in some lymphocytes but not others may reflect the state of activation of the lymphocytes.     

Inorganic phosphate treatment of nephrolithiasis

We report the results of long-term inorganic phosphate therapy in 47 patients suffering from recurrent calcium-containing urinary calculi. Forty-five patients had hypercalciuria before treatment. Phosphate therapy had no effect on urinary calcium excretion or stone passage but did appear to reduce the need for lithotomy. The stone passage-removal rate in the 5 years before therapy was 1.3 per patient per year and fell to 0.8 in the years of treatment (mean 5.5 years). The lithotomy rate fell from 0.12 per patient per year to 0.04 with treatment (p < 0.01). Patients who were free of stones at the start of the therapy fared best. Significant decreases in serum alkaline phosphatase were noted in many patients, possibly a sign of healing subclinical osteomalacia.