PubMed Health⌕ Search

Biomedical subjects

H Shubin

Publications and source records attributed to H Shubin.

At least 19 recordsLinked to original sources
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↗
PubMed1975

Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction.

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.

Adult↗
PubMed1975

Pulmonary edema during volume infusion.

The relationship between left ventricular filling pressure and plasma colloid osmotic pressure to pulmonary edema was examined in a group of 37 patients, the majority of whom were hypovolemic. Sixteen patients developed pulmonary edema during fluid infusion. In the 21 patients who did not develop pulmonary edema, the left ventricular filling pressure was slightly elevated but the colloid osmotic pressure was not reduced. The majority of these patients were treated with colloid solutions (group I). In five of the 16 patients who developed pulmonary edema, the left ventricular filling pressure was elevated and there was no reduction in the plasma colloid osmotic pressure. These patients received only colloids (group II). In the other 11 patients who developed pulmonary edema, the left ventricular filling pressure was normal but the plasma colloid osmotic pressure was reduced to 16 +/- 2 torr (group III). The colloid osmotic pressure in this group was significantly less than in the other two groups (P less than 0.01). Most of these patients received large volumes of crystalloid solutions. After administration of furosemide, clearing of pulmonary edema in this group was associated with normalization of the plasma colloid osmotic pressure. Infusion of large volumes of crystalloids in hypovolemic patients can be hazardous, for reduction of the plasma colloid osmotic pressure may predispose to the development of pulmonary edema even when the left ventricular filling pressure remains normal.

Adult↗
PubMedDate not supplied

Reduction in colloid osmotic pressure associated with fatal progression of cardiopulmonary failure.

The relationship between colloid osmotic pressure (COP) and the severity of cardiopulmonary failure was investigated in 99 consecutive patients admitted to our Shock Unit including 41 survivors and 58 fatal cases. The COP was significantly lower (p less than 0.001) in fatal cases in comparison to survivors. None of 21 patients in whom COP was less than 10.5 torr survived. A progressive increase in survival with typical S-shaped distribution was observed as COP increased from 10 to 19 torr, above which all patients survived. These preliminary observations demonstrated that reduction in COP in critically ill patients is associated with increases in mortality. The mechanisms by which lowering of COP may be related to fatal progression of cardiopulmonary failure is the subject of continuing study.

Adolescent↗