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Biomedical subjects

S C Haskins

Publications and source records attributed to S C Haskins.

At least 19 recordsLinked to original sources
PubMed2000

Weaning from mechanical ventilation.

Patients that require positive pressure ventilation to maintain sufficient alveolar ventilation or pulmonary gas exchange may eventually reach a point in the course of their care wherein mechanical ventilation is no longer necessary. This process of transferring the work of breathing from the ventilator back to the patient is referred to as ventilator weaning. The term "ventilator weaning" may be used to refer to all methods by which this transfer of workload may be accomplished. In many patients, particularly those with short-lasting or readily correctable causes of respiratory insufficiency (e.g., general anesthesia), the discontinuation of positive pressure ventilation may be easily achieved. Indeed, in patients awakening from general anesthesia, the axiom "awake enough to blink, awake enough to breath" may prove to be a sufficient guideline. However, in those patients requiring long-term mechanical ventilatory support, the process can prove to be both frustrating and exceptionally challenging. It is of crucial importance to identify those patients that may be successfully weaned because of both the financial impact of prolonged intensive care unit hospitalization and the risks imposed on the patient by the process of positive pressure ventilation. To be able to predict which patients may be ready to be weaned from the ventilator requires an understanding of the balance between the work of breathing (ventilatory load) and the ability of the patient's respiratory pump to meet those needs (ventilatory capacity). The management of patients experiencing difficulty during the weaning process requires that the clinician recognize imbalances between ventilatory load and capacity and to correct these imbalances once identified.

Algorithms↗
PubMed1999

Haemodynamic effects of ATP in dogs during hypoxia-induced pulmonary hypertension.

Pulmonary hypertension may result from an increase in vascular resistance caused by persistent hypoxia. We have investigated the effects of adenosine triphosphate (ATP), administered into the pulmonary artery, on haemodynamic changes occurring in anaesthetized adult dogs subjected to acute hypoxic pulmonary vasoconstriction. Hypoxia alone (ventilation with 10% O2/90% N2) caused significant increases in mean pulmonary arterial blood pressure (PAP), central venous pressure (CVP), and cardiac index (CI) by 71, 102 and 38%, respectively. ATP (0.03-3.0 micromol/kg/min approximately 0.02-1.65 mg/kg/min), when infused under hypoxic conditions, significantly reduced both mean PAP and systemic arterial blood pressure (ABP) in a dose-dependent manner. The maximum decrease in mean PAP amounted to 20%; mean ABP, on the other hand, was decreased by up to 52% (P<0.01). Heart rate, CI, CVP and pulmonary occlusion pressure were not dose-dependently affected by ATP. Our data indicate that while pulmonary arterial administration of ATP in mature dogs during hypoxic pulmonary hypertension causes dilation in the pulmonary vascular bed, it is even more effective in dilating the systemic vasculature. This result suggests a need for further evaluation and warrants cautious use of ATP in the treatment of hypoxic pulmonary hypertension in adult dogs.

Adenosine Triphosphate↗
PubMed1999

Deep sedation and mechanical ventilation without paralysis for 3 weeks in normal beagles: exaggerated resistance to metocurine in gastrocnemius muscle.

BACKGROUND: Patients in the intensive care unit may have muscle weakness in the recovery phase, and disuse atrophy may play a role in this weakness. To assess this problem, the authors measured changes in the potency of the nondepolarizing neuromuscular blocking agent metocurine in a canine model that involved 3 weeks of intensive care, nonparalyzing anesthesia with pentobarbital, and positive-pressure ventilation. METHODS: Six dogs were anesthetized with pentobarbital to a sufficient depth that spontaneous and reflex muscle movements were absent. Their tracheas were intubated, their lungs were mechanically ventilated, and they received round-the-clock intensive medical and nursing care for 3 weeks. Transduced gastrocnemius muscle responses to metocurine were determined weekly. A 4- to 15-min infusion of 148-4,300 microg/min (longer durations and greater concentrations on progressive weeks) yielded more than 80% paralysis. Serial metocurine plasma concentrations during the onset of the block and recovery provided data to determine pharmacokinetics using NONMEM. Metocurine plasma concentrations and the degree of paralysis were used to model the effect compartment equilibration constant, and the Hill equation was used to yield the slope factor and potency within the effect compartment. RESULTS: The metocurine effect compartment concentration associated with a 50% diminution of twitch height after 3 weeks was 1,716+/-1,208 ng/ml (mean +/- SD), which was significantly different from 257+/-34 ng/ml, the value on day 0. There were no pharmacokinetic differences. CONCLUSION: The absence of muscle tone and reflex responsiveness for 3 weeks was associated with exaggerated resistance to the neuromuscular blocker metocurine.

Animals↗
PubMed1998

Plasma electrolyte and metabolite concentrations associated with pentobarbital or pentobarbital-propofol anesthesia during three weeks' mechanical ventilation and intensive care in dogs.

Propofol and pentobarbital were used for deep sedation during prolonged mechanical ventilation (3 weeks) and nutritional supplementation in 17 clinically normal dogs in an intensive care setting. Tolerance developed to both drugs. Propofol, in combination with pentobarbital, at an infusion rate of 75 micrograms/kg of body weight per minute was preferred. Pentobarbital infusion alone, begun at the rate of 5 to 6 mg.kg-1.h-1, was satisfactory. The combination of both drugs provided smooth, stable anesthesia and required minimal interventions by intensive care unit personnel. Blood gas tensions and electrolyte, parathyroid hormone (PTH), and metabolite concentrations were generally stable throughout, unless condition of the dog deteriorated (e.g., infection, pneumothorax). Hematocrit and red blood cell count decreased with time, likely attributable principally to multiple blood sample collections. White blood cell count, alkaline phosphatase, phosphate, fibrinogen, cholesterol, and triglyceride values increased with time, in association with pentobarbital and the combination of pentobarbital and propofol. Some of these changes appear to have been related to generic responses to stress and inflammation, some to altered metabolism, and some to the lipid solvent of propofol. The increase in triglyceride concentration was greater when propofol was used. Mortality was 47%, with death occurring between days 2 and 18.

Anesthesia, Intravenous↗
PubMed1994

The cardiovascular sparing effect of fentanyl and atropine, administered to enflurane anesthetized dogs.

Cardiovascular effects of high dose opioid together with low dose inhalant were compared with inhalant alone to determine whether opioid/inhalant techniques were less depressant on the cardiovascular system. The effects of positive pressure ventilation and increasing heart rate to a more physiological level were also studied. Cardiovascular measurements recorded during administration of enflurane at 1.3 minimum alveolar concentration (MAC; 2.89 +/- 0.02%) to spontaneously breathing dogs (time 1) and during controlled ventilation [arterial carbon dioxide tension at 40 +/- 3 mmHg (time 2)] were similar. At time 2, mixed venous oxygen tension and arterial and mixed venous carbon dioxide tensions were significantly decreased, while arterial and mixed venous pH were significantly increased compared to measurements at time 1. After administration of fentanyl to achieve plasma fentanyl concentration of 71.7 +/- 14.4 ng/mL and reduction of enflurane concentration to yield 1.3 MAC multiple (0.99 +/- 0.01%), heart rate significantly decreased, while mean arterial pressure, central venous pressure, stroke index, and systemic vascular resistance index increased compared to measurements taken at times 1 and 2. Pulmonary arterial occlusion pressure was significantly increased compared to measurements taken at time 2. After administration of atropine until heart rate was 93 +/- 5 beats/min (plasma fentanyl concentration 64.5 +/- 13.5 ng/mL) heart rate, mean arterial pressure, cardiac index, oxygen delivery index, and venous admixture increased significantly compared to values obtained at all other times.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Cardiopulmonary effects of halothane in hypovolemic dogs.

Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 +/- 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The case for in circuit vaporizers.

In circuit vaporizers have some characteristics that differ from out of circuit vaporizers. In circuit vaporizers are easy to use, effective, and offer several clinical advantages.

Anesthesia, Inhalation↗
PubMed1992

Breathing circuits.

Explore the source record for details and available documents.

Anesthesia, Closed-Circuit↗