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Dive into the research topics where Herbert Shubin is active.

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Featured researches published by Herbert Shubin.


Circulation | 1971

Cardiac Arrest in the Critically Ill I. A Study of Predisposing Causes in 132 Patients

Samuel J. Camarata; Max Harry Weil; Paul K. Hanashiro; Herbert Shubin

The events preceding cardiac arrest were investigated in 132 critically ill patients on the basis of the hemodynamic, respiratory, and metabolic status prior to cardiac arrest. Approximately one-half of the patients had respiratory acidosis prior to cardiac arrest and only one of these patients ultimately survived. An additional one-fourth had metabolic acidosis due to progressive perfusion failure (shock), and none survived. In the remaining one-fourth, an immediate catastrophic and potentially preventable event accounted for cardiac arrest, and all but one of the long-term survivors were included in this group. In thirteen patients, obstruction or dislodgment of endotracheal tracheostomy tubes, or interruption of ventilation, was recognized as the immediate cause. In an additional 20 patients, cardiac arrest was associated with an adverse effect of a drug. Twelve instances of cardiac arrest were associated with central venous injection of aminophylline.The initial cardiac resuscitation attempt was effective in 38% of patients. However, the majority of patients who survived the first episode succumbed after a second or third episode. The cumulative survival was disappointingly small. Only six patients, or 5% of the total group of 132 patients, were long-term survivors. These data may provide the basis for more restricted use of routine and repetitive resuscitative measures particularly for elderly patients in whom acidemia is due to progressive ventilatory or circulatory failure.


The American Journal of Medicine | 1974

Cardiac arrest in the critically III: II. Hyperosmolal states following cardiac arrest

Joao A. Mattar; Max Harry Weil; Herbert Shubin; Leon Stein

Abstract A hyperosmolal state was documented in 12 patients after cardiac resuscitation. Plasma osmolality was increased to levels which are regarded as potentially lethal on the basis of experimental and clinical studies. The hyperosmolal state was directly related to injection of Hypertonic sodium bicarbonate (7.5 per cent) in amounts ranging from 90 to 540 mOsm. All 12 patients died. On the basis of these observations, we recommend caution in using large amounts of hypertonic sodium bicarbonate for acute cardiac resuscitation. The routine and repetitive measurement of blood pH and carbon dioxide pressure, and measurement of plasma osmolality during the resuscitative period, are advised to guide the use of alkali in order to avoid the iatrogenic risk of fatal hyperosmolal states.


Critical Care Medicine | 1973

Quantitation of severity of critical illness with special reference to blood lactate.

Lee D. Cady; Max Harry Weil; Abdelmonem A. Afifi; Sybil F. Michaels; Vinnie Y. Liu; Herbert Shubin

A total of 410 critically ill patients in critical care units of six community hospitals were surveyed for a period of 31 days. A prognostic index of survival was derived by discriminant function analysis utilizing measurement of blood lactate, blood pressure, heart rate, arrhythmias, spontaneous respiration, urine volume, body temperature, age, and a five-point rating of clinical condition by the nursing staff. The case fatality rate in patients in whom blood lactate exceeded 2.7 mM was 50% fatality rate was 5% when lactate was less than 2.7 mM. The best prediction of survival was obtained by combining the plasma lactate and the five-point rating of the patients condition. These data therefore could serve as a measure of the severity of illness at the time of admission and provide a quantitative guide for objective comparison of the effectiveness with which critical care services are delivered in acute care units. They can also provide an objective basis for priority assignment to cardiac care, intensive care, and other specialized units of the hospital


Circulation | 1975

Pulmonary edema during volume infusion.

Leon Stein; Jean-Jacques Beraud; M Morissette; Protásio Lemos da Luz; Max Harry Weil; Herbert Shubin

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 < 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.


Advances in Experimental Medicine and Biology | 1972

Proposed Reclassification of Shock States with Special Reference to Distributive Defects

Max Harry Weil; Herbert Shubin

Some years ago, for lack of better knowledge, most of us were tempted to classify shock on an etiologic basis. We referred to: (a) shock due to blood loss (hypovolemic shock); (b) cardiogenic shock (pump failure); (c) bacterial shock (bacteremia, endotoxin); (d) acute hypersensitivity reactions (anaphylactic shock); (e) neurogenic shock (barbiturate and narcotic overdose, transection of the spinal cord; (f) shock associated with obstruction to blood flow, e. g., pulmonary embolization; and (g) endocrine forms of shock (myxedema, pheochromocytoma, adrenocortical insufficiency, insulin excess).


Critical Care Medicine | 1974

Routine plasma colloid osmotic pressure measurements.

Max Harry Weil; Martin Morissette; Sybil Michaels; Joe Bisera; Edward Boycks; Herbert Shubin; Edwin Jacobson

A method for routine determination of colloid osmotic pressure (COP) in the clinical laboratory is described. A transducer membrane system is utilized in which the colloid osmotic pressure (COP) of fresh or refrigerated plasma or albumin is compared to that of isotonic saline. The measurement is completed within an average period of less than four minutes. Duplicate measurements demonstrated high reproducibility (r = >.95) and reference measurements obtained over a period of ten months were consistently within a range of 1 torr. Heparin in excess of 200 units/ml delayed equilibration. Values obtained in normal ambulatory and supine subjects conform closely to those previously reported.


Critical Care Medicine | 1975

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

Martin Morissette; Max Harry Weil; Herbert Shubin

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< 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.


The New England Journal of Medicine | 1971

Accumulative Prognostic Index for Patients with Barbiturate, Glutethimide and Meprobamate Intoxication

Abdelmonem A. Afifi; Susan T. Sacks; Vinnie Y. Liu; Max Harry Weil; Herbert Shubin

Abstract To assess and update prognosis in a group of critically ill patients, repetitive measurements of physiologic status were made in 52 patients who were comatose and in shock after attempting suicide by ingesting large doses of barbiturate, glutethimide or meprobamate. Only three variables were needed to provide the prognostic information contained in all 25 variables measured. A momentary prognostic index, which estimates the patients probability of survival on the basis of a single set of measurements, and an accumulative prognostic index, which takes into account previous sets of measurements, were derived. The accumulative prognostic index may provide a more realistic assessment of prognosis, for it de-emphasizes transient fluctuations in the patients condition and emphasizes directional changes as a function of time. Formulas were derived that permit calculation of this index by the clinician with the use of a desk-top calculator.


American Journal of Cardiology | 1960

Cardiovascular findings in children with sickle cell anemia

Herbert Shubin; Ruebin Kaufman; Morse Shapiro; David C. Levinson

Abstract Cardiovascular findings are described in seven children with sickle cell anemia. Clinically the following features were noted: (1) exertional dyspnea and fatigue; (2) wide fixed splitting of the second heart sound; (3) third “filling” heart sound in five of the seven cases; (4) systolic murmur of grade II intensity or louder, most prominent over the upper left sternal border; (5) roentgenographic evidence of diffuse cardiomegaly and increased pulmonary vascularity; (6) abnormal electrocardiograms in four cases. Laboratory findings of note were: (1) hemoglobins from 6.3 to 9.5 gm. per cent and hematocrit readings from 18 to 27 volumes per cent; (2) increased total blood volumes and plasma volumes in five of six patients. Right heart catheterizations in these patients revealed the following: (1) normal vena caval, right atrial, pulmonary artery and wedged pulmonary artery pressures; (2) normal or low pulmonary vascular resistances at rest and with exercise; (3) cardiac indices averaging twice normal; (4) increased stroke indices; (5) arterial oxygen unsaturation at rest and after breathing 100 per cent oxygen in all cases; (6) relatively small arteriovenous oxygen differences at rest and with exercise; (7) relatively high coronary sinus oxygen saturations; (8) an abnormal Valsalva response.


Critical Care Medicine | 1977

The measurement of the work of breathing for the clinical assessment of ventilator dependence

Robert J. Henning; Herbert Shubin; Max Harry Weil

The work of breathing was measured in 10 normal subjects and in 28 critically ill patients with acute complications of obstructive pulmonary disease treated with assisted ventilation. The measurement of the work of breathing was found to be a useful objective variable for determining the capability for independent ventilation. Dependence on mechanical ventilation was observed when the respiratory work was ≥1.7 kg · m/min. Patients were ordinarily capable of spontaneous ventilation when the respiratory work was ≤1.0 kg · m/min. Discontinuation of assisted ventilation was likely to be successful in those patients whose respiratory work was ≤ 1.5 kg · m/min if the patient was able to increase and maintain his work capability by a factor of two when breathing against an inspiratory resistance of 5 cm H2O for 10 min. Failure to increase the respiratory work when breathing against an inspiratory resistance indicated limitations in respiratory mechanics and was associated with the need for prolonged assisted ventilation. The measurement of the work of breathing against an inspiratory resistance of 5 cm H2O was useful in the identification and quantification of ventilatory reserve in patients with obstructive pulmonary disease.

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Max Harry Weil

University of Southern California

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Leon Stein

University of Southern California

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Jose Cavanilles

University of Southern California

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David C. Levinson

University of Southern California

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Norman Palley

University of Southern California

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Jean-Jacques Beraud

University of Southern California

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Susan T. Sacks

University of Southern California

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Sybil Michaels

University of Southern California

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Vinnie Y. Liu

University of Southern California

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