Search PubMed⌕ Search

Biomedical subjects

H Shubin

Publications and source records attributed to H Shubin.

At least 19 recordsLinked to original sources
PubMed1982

Oxygen transport, consumption and utilization during barbiturate intoxication.

Factors related to oxygen availability and requirements were measured on 51 occasions in 14 patients intoxicated with short-acting barbiturates. Patients had no clinical signs of circulatory shock. The cardiac index was normal (3.4 +/- 1.1 1/min/m2) but there was a slight decrease of the mean arterial oxygen content (17.2 +/- 3.0 ml/100 ml). Oxygen transport was normal (571 +/- 199 ml/min/m2). However, the arteriovenous oxygen differences were decreased (3.4 +/- 1.0 ml/100 ml). Oxygen consumption was reduced (110 +/- 42 ml/min/m2) and the oxygen extraction ratio (oxygen consumption/oxygen transport) was decreased (0.20 +/- 0.05), thus confirming a decreased oxygen utilization. Arterial concentration of lactate was normal. Accordingly the observed decrease in oxygen consumption was related to a reduction in oxygen requirements during barbiturate intoxication rather than due to an imbalance between availability and metabolic requirements for oxygen.

Adolescent↗
PubMed1981

Abnormal temperature control after intoxication with short-acting barbiturates.

Changes in rectal and toe temperatures were measured in 16 patients who had been intoxicated with short-acting barbiturates. The lowest temperatures observed in the group of 16 patients averaged 35.5 +/- 2.0 degrees C. In 11 patients, the interval between intoxication and admission was documented. There was a significant correlation (r = 0.83) between the time of estimated intoxication and hypothermia. Patients who were admitted soon after the ingestion of the barbiturates had the lowest rectal temperatures. These observations indicate that hypothermia is a usual clinical sign in the initial period after intoxication with a short-acting barbiturate. Except for 2 patients, rectal temperature exceeded 38 degrees C during the interval of recovery with the maximum rectal temperature averaging 39.0 +/- 0.8 degrees C. Hyperthermia was not related to infection of the airways, lungs, urinary tract, or bloodstream. In 11 patients, pathogenic organisms were recovered from the airway and/or urine, but there was no difference in the highest rectal temperature in these patients (39.0 +/- 0.9 degrees C) when compared with 5 patients from whom no pathogenic organisms were recovered (39.2 +/- 0.7 degrees C). Accordingly, there was no evidence that hyperthermia was due to infection. The skin temperatures of the ventrum of the first toe were not typically decreased during hypothermia. To the contrary, increases in skin temperatures were often observed during hypothermia. These observations provide evidence of altered thermoregulation with increased surface heat loss accounting for the hypothermia in the early course and heat conservation with hyperthermia during the later course of intoxication by short-acting barbiturates.

Adolescent↗
PubMed1977

Afterload reduction with phentolamine in patients with acute pulmonary edema.

Phentolamine in amounts of 10 to 40 microgram/kg/min was infused intravenously for the emergency treatment of acute pulmonary edema due to left ventricular failure. Fourteen patients with arteriosclerotic heart disease, ranging in age from 52 to 87 years, had clinical and roentgenographic signs of pulmonary edema. The pulmonary artery wedge pressure was increased to an average of 24 mm Hg and the cardiac index was decreased to 1.9 liters/min/m2 or less prior to the administration of phentolamine. A reduction in the pulmonary artery wedge pressure to 14 mm Hg and an increase in the cardiac index to 2.5 liters/min/m2 was observed in response to this alpha adrenergic blocking agent. Reduction in peripheral resistance with phentolamine was associated with reversal of pulmonary edema.

Acute Disease↗
PubMed1977

Bacterial shock.

Bacterial shock due to Gram-negative bacilli is best managed by prompt control of the infection with appropriate antibiotics and surgical drainage or excision. Corticosteroids for purposes of controlling systemic reactions to bacteria and their toxins constitute adjunctive therapy. Volume repletion and respiratory support may be of the greatest importance for temporary support of these critically ill patients. Vasoactive drugs including dopamine and isoproterenol should be used very sparingly and only as very temporary expedients.

Anti-Bacterial Agents↗
PubMed1976

Bacterial shock.

Explore the source record for details and available documents.

Adrenal Cortex Hormones↗
PubMed1976

Relationship between pulmonary hemodynamics and arterial pH and carbon dioxide tension in critically ill patients.

To ascertain the clinical significance of derangements in arterial pH and arterial carbon dioxide tension (PaCO2) in modifying pulmonary arterial pressures and pulmonary vascular resistance in critically ill patients, the relationship between these two sets of variables was evaluated in 75 patients. No significant differences in pulmonary hemodynamic values were found among patients with acidemia, a normal pH, or alkalemia, even at extreme pH values; and there was no consistent relationship between PaCO2 and each of the pulmonary hemodynamic measurements. In patients who initially had a normal pH but subsequently developed acidemia or alkalemia, there was also no significant correlation between changes in pH and pulmonary hemodynamic values. We conclude that abnormalities of pulmonary hemodynamic values in seriously ill patients are usually due to factors other than acid-base derangements. Of practical importance is the observation that the predictability of the pulmonary arterial wedge pressure from the pulmonary arterial diastolic pressure is not invalidated by acid-base disturbances.

Acid-Base Imbalance↗
PubMed1975

Treatment of circulatory shock. Use of sympathomimetic and related vasoactive agents.

Reduction of effective blood flow represents the primary disturbance accounting for circulatory shock. Four categories of circulatory shock are identified: cardiogenic, hypovolemic, distributive, and obstructive. The pharmacology and clinical implications for treatment of shock with vasoactive drugs are reviewed in this context. Except for epinephrine, when it is used for treatment of anaphylactic shock, there is no specific indication for the routine use of alpha- or beta-adrenergic receptor agonists. These agents may increase blood pressure or cardiac output, but nutritive flow is not necessarily improved. Comparable limitations are observed with alpha-adrenergic receptor blocking agents. However, selective effects on the myocardium and on the resistance, exchange, and capacitance vessels may be advantageous as an interim and complementary measure. Since vasoactive drugs frequently intensify the fundamental defect accounting for perfusion failure, their selective rather than routine employment is mandatory.

Adrenergic alpha-Agonists↗
PubMed1975

Oxygen delivery, anoxic metabolism and hemoglobin-oxygen affinity (P50) in patients with acute myocardial infarction and shock.

Changes in systemic oxygen delivery after acute myocardial infarction were investigated in 21 patients. In seven patients with shock, circulatory failure was characterized by a significant reduction in cardiac index, a decrease in oxygen transport and oxygen consumption and an increase in concentration of blood lactate; a decrease in the affinity of hemoglobin for oxygen (increased P50) was also noted. The P50 averaged 28.8 plus or minus 0.87 (standard error of the mean) torr in patients with shock and 26.0 plus or minus 0.45 torr (P less than 0.05) in patients without circulatory failure. However, there was no significant difference in oxygen extraction from arterial blood between the two groups. The time course of the changes in P50, cardiac index and oxygen consumption was separately examined in 12 patients. In six patients with shock, P50 increased by an average of 4.6 plus or minus 2.05 torr (P less than 0.05) and this augmentation accounted for an estimated 18 percent increase in oxygen release. Maximal P50 values were observed after 24 hours of circulatory failure. In the absence of shock, no consistent changes in P50, cardiac index or oxygen consumption were observed. These data indicate that a reduction in oxygen delivery after acute myocardial infarction is followed by a compensatory increase in P50. This change in P50 accounts for increases in oxygen availability independently of changes in cardiac output.

Aged↗
PubMed1975

Blood P50 calculated from a single measurement of pH, PO2, and SO2.

P50 was calculated from a single measurement of pH, Po2, and So2 at a known temperature in 135 blood samples from 21 normal nonsmokers and eight patients. In the 92 blood samples with So2 between 20 and 90 per cent, the standard deviation of repeated calculated P50's on the same sample of blood at different So2 was plus or minus 1.0 Torr. Below So2 of 20 per cent and above So2 of 90 per cent, the standard deviations were plus or minus 5.5 and plus or minus 2.4 Torr, respectively. Combined measurement errors of plus or minus 1 Torr in Po2, plus or minus 1 percent in So2, plus or minus 0.01 in pH, and plus or minus 0.1 degree C in temperature are sufficient to explain the observed variation in calculated P50 in 90 per cent of 135 blood samples from 29 subjects and account for the greater observed variation at So2 less than 20 per cent and greater than 90 per cent.

Carbon Dioxide↗