Biomedical subjects
Publications and source records attributed to A Perel.
A pop-off valve system for use with intermittent mandatory ventilation that employs high flow and a reservoir bag is described. It ensures constancy of the mechanical tidal volume regardless of the flow rate of fresh gases into the reservoir bag of the spontaneous breathing circuit.
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Simple insertion of a nasogastric (NG) tube was successful in only 52 of 100 anesthetized intubated patients. After the larynx was manually pulled forward, the NG tube was successfully inserted in 33 patients. In the remaining 15 patients, the NG tube was inserted only with the aid of a finger or a laryngoscope used with Magill forceps. The difficulty of NG tube insertion was not correlated with sex, age, weight, or type of endotracheal intubation. Forward displacement of the larynx by manually gripping and lifting the thyroid cartilage is a useful and safe maneuver that facilitates NG tube insertion in anesthetized intubated patients.
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We describe continuous positive airway pressure (CPAP) by mask to reduce hypercarbia in two patients who had pulmonary edema due to congestive heart failure. In such patients, beside reducing venous return and filling pressures, CPAP improves compliance and decreases the work of breathing, thereby improving effective ventilation. Hence, CPAP may be useful to combat not only hypoxemia but also hypercarbia that is associated with pulmonary edema.
The establishment of apnea for the diagnosis of brain death by disconnecting the patient from the ventilator may lead to dangerous hypoxemia at the end of the test period. We established apnea for 4 min in 8 patients with suspected brain death, both by disconnecting them from the ventilator after 10 min ventilation with FIO2 = 1.0 (method "A"), and by leaving them attached to an IMV ventilator circuit with a continuous flow of 100% O2 and PEEP of 4-8 cm H2O without mechanical ventilation (method "B"). PaO2 decreased during the apneic period by 143 +/- 65 (SD) mmHg using method "A", and by 48 +/- 28 mmHg using method "B" (p less than 0.002). The changes in PaCO2 and pH were similar following both apneic methods. We conclude that it is safer to test for apnea by leaving the patients on a continuous flow of 100% oxygen and low PEEP than to disconnect them from the ventilator.
We report two cases of children, 7 and 14 yr old, in whom prolonged infusion of thiopental sodium (TS) was used to control intracranial hypertension previously unresponsive to conventional therapy. Intracranial hypertension followed removal of a large tumor in 1 case, and trauma in the other. TS was administered at a rate of up to 7 mg/kg . h for 8 days in 1 patient, and up to 12 mg/kg . h for 10 days in the other. Both children regained consciousness and made significant recovery of neurological function. The advantage and the side-effects of the prolonged use of TS for intracranial hypertension are discussed.
Fourteen dogs were anesthetized, intubated, and breathed room air spontaneously. We then instilled 2 ml/kg of fresh nonheparinized donor blood into their tracheas. Seven dogs received no treatment and served as controls (group A); respiratory rate (RR) increased from 25 +/- 11 (mean +/- SD) to 103 +/- 33 breath/min, HR decreased from 179 +/- 28 to 136 +/- 42 beat/min, PaO2 decreased from 82 +/- 10 to 30 +/- 4 torr, pulmonary venous admixture (Qsp/Qt) increased from 0.14 +/- 0.10 to 0.72 +/- 0.06, and venous oxygen tension (PVO2) decreased from 46 +/- 4 to 22 +/- 5 torr 10 min after the aspiration of blood; all changes were statistically significant (p less than .05). After 4 h, RR and HR returned to control values, but PaO2 was only 58 +/- 10 torr. Cardiac output, oxygen consumption (VO2), and pulmonary and systemic BP and resistances were not significantly affected. Thirty-five min after the other 7 dogs aspirated blood (group B), 10 cm H2O of continuous positive airway pressure (CPAP) was applied while they breathed spontaneously. CPAP reduced Qsp/Qt to 0.31 +/- 0.10 and 0.15 +/- 0.11 30 and 90 min after its application, respectively (p less than .05). By 4 h, the PaO2 of group B dogs was 81 +/- 15 torr (p less than .05 compared with group A). CPAP also increased arteriovenous oxygen content difference (C[a-v]O2) compared with the nontreated dogs. Four hours after the aspiration of blood, all dogs were extubated. Twenty-four hours later, arterial blood gases were normal in all dogs of both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
The possible value of albumin in a rabbit model of the acid aspiration syndrome was studied. Hydrochloric acid was instilled into the respiratory tracts of three groups of rabbits: Group A received a high intravenous dose of human albumin (1.5 gm/kg body weight); Group B (control) was given Hartmann's solution, and Group C a low dose of albumin (0.25 gm/kg body weight). The total amount of intravenous fluids was identical in all groups. Serum and pulmonary edema fluid (PEF) concentrations of total protein were highest in Group A. Simultaneous concentration gradients between serum and PEF for total protein, human and rabbit albumin, and globulin fractions were not statistically different in the three groups. In Group A, PEF appeared first and PaO2, static compliance, and hematocrit decreased significantly more than those of the two other groups. Survival of animals in Group C was highest. An additional Group (D) of rabbits received the same high dose of albumin without acid aspiration. In Group D hematocrit decreased while serum total protein and pulmonary function remained unchanged. It seems that a high dose of albumin causes a further deterioration of lung function following acid aspiration because of extravasation into the interstitial space. The administration of low doses of albumin was not different than Hartmann's solution, but led to the best survival in our model.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The authors studied 86 consecutive patients admitted to the ICU after severe head trauma. Of these, 19 nondiabetic patients developed persistent nonketotic hyperglycemia (NKH), defined as plasma glucose greater than 270 mg/dl (15 mM/L), 1.7 +/- 1.1 (SD) days after injury. When NKH occurred, all patients were in very deep coma (Glasgow Coma Scale score 3), and when intracranial pressure (ICP) was measured (12 patients), its mean value was 59.8 +/- 20.4 mm Hg. Although 11 of 19 patients had associated diabetes insipidus (DI), NKH was not related to increased fluid and glucose loading. All patients with NKH died (mean time of survival after NKH was 2.1 +/- 1.4 days) in contrast to a 17.1% early mortality rate in patients with severe head injury without NKH. The authors could not show a direct correlation between the height of ICP and the level of blood glucose.
We studied the effects of uneven pulmonary artery obstruction by microemboli on steady state transvascular fluid and protein exchange in normal and leukopenic sheep. We measured pulmonary artery and left atrial pressures, cardiac output, lung lymph flow, and lymph plasma protein concentrations. Sheep were made profoundly leukopenic by administration of intra-arterial mechlorethamine hydrochloride (0.4 mg/kg, two doses) and colchicine (0.1-0.2 mg/kg, anesthetized sheep only). In anesthetized sheep, we injected glass beads 200 micrometers in diameter via the right atrium to raise pulmonary vascular resistance to 2-3 times baseline values. With normal levels of circulating leukocytes, sheep developed an increased protein-rich lymph flow from the lung characteristic of increased permeability edema. Leukopenic sheep had a significantly attenuated response after embolization for equivalent degrees of vascular obstruction. In unanesthetized sheep, we continuously infused air bubbles 1 mm in diameter via the right atrium to raise pulmonary vascular resistance to about 2 times baseline values. Each sheep served as its own control. With normal circulating leukocyte levels, there was an increase in protein-rich lymph flow from the lung during embolization. When the air infusion ended, the sheep recovered to the baseline condition in 24 hours. We induced emboli with the same amount of air when the sheep were profoundly leukopenic; lymph and protein flow from the lung were significantly less for equivalent degrees of obstruction. We conclude that circulating leukocytes are essential for the microvascular injury that results in increased permeability in the lungs of sheep after microembolization.
Two patients with imminent gangrene of the extremities caused by ergot-induced arteriospasm underwent mechanical dilatation of the arteries when conventional measures such as anticoagulation, vasodilation, and sympathetic blockade produced no improvement. Dilatation by a balloon-tipped catheter produced an immediate and sustained reversal of the arteriospasm, together with a dramatic relief of symptoms and signs.
To test whether platelets are necessary for the increased vascular permeability associated with microemboli, we used 16 anesthetized sheep in which we measured lung lymph flow, pulmonary arterial and left atrial pressures, thermodilution cardiac output, and lymph/plasma protein concentration. Injecting glass bead microemboli (200 micrometers diam) until pulmonary vascular resistance increased to three times base-line values caused lung lymph flow to increase at nearly constant lymph-to-plasma protein concentration ratio that is characteristic of increased microvascular permeability. Antiplatelet serum alone caused transient increases in pulmonary vascular resitance and lung lymph flow, but produced no change in steady-state lung fluid balance. After depleting platelets by greater than 97%, tripling pulmonary vascular resistance with emboli resulted in increases in lung lymph and protein flow comparable to that seen in untreated sheep. We injected twice the amount of beads in thrombocytopenic sheep compared to untreated sheep. We conclude that, although platelets do augment the pulmonary hypertension after emboli, they are not essential for the microemboli vascular injury.
We measured the regional distribution of pulmonary extravascular water to test our prediction that, because of higher vascular hydrostatic pressure in more dependent zones, the bottom of the lung would tend to be wetter than the top. We injected eight normal sheep under halothane anesthesia with 125I-labeled albumin and killed them 5 min later. We suspended the sheep in the prone position and froze them solid in dry ice. We sawed the thorax into horizontal slices, chipped the frozen lung from each, and determined extravascular lung water and hematocrit. Hematocrit was calculated from separately measured red blood cell (tissue hemoglobin) and plasma (125I-albumin) masses. We found regional extravascular water was constant throughout the lung. Regional hematocrit was significantly higher at the lung base than at the apex in these slowly frozen sheep after death. Calculation of extravascular water using a single blood mass marker (hemoglobin) underestimated lung water, more so at the base than at the apex, because blood mass was overestimated. Accurate measurement of blood mass is critical in the calculation of regional lung water.