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Biomedical subjects

J P Howe

Publications and source records attributed to J P Howe.

8 recordsLinked to original sources
PubMed1991

Cardiovascular effects of intravenous clonidine. Partial attenuation of the pressor response to intubation by clonidine.

The effect of clonidine on the pressor and heart rate response to tracheal intubation was studied in a placebo-controlled, randomised, double-blind trial. Thirty patients were pretreated with either clonidine 1.25 micrograms/kg, or clonidine 0.625 microgram/kg or an equivalent volume of normal saline, given intravenously 15 minutes before induction of anaesthesia. The attenuation of the pressor response to intubation of both clonidine groups was statistically significant compared to the saline group. Neither dose of clonidine completely abolished the increase in either heart rate or blood pressure. There was no difference in attenuation between the clonidine treatments; this indicated that the lower dose may be the more appropriate.

Adult↗
PubMed1991

The effect of intravenous clonidine on the forearm circulation.

The effect of two doses of clonidine on forearm blood flow was compared with an inert treatment using mercury strain gauge venous occlusive plethysmography. In the clonidine treated groups, forearm blood flow was unaffected in the resting state, but decreased sharply with tracheal intubation. In the saline group, blood flow increased with intubation. Forearm vascular resistance increased in the clonidine treated groups, but decreased in the saline group. These results suggest that clonidine has a peripheral action in anaesthetised normotensive individuals, and is not a purely centrally acting drug.

Adult↗
PubMed1978

Basic life support.

Explore the source record for details and available documents.

Education, Medical↗
PubMed1977

Pulmonary embolism, pulmonary hemorrhage and pulmonary infarction.

We compared 41 patients with angiographic proof of pulmonary embolism and clinical signs of pulmonary infarction (as evidenced by an infiltrate on x-ray study and pleuritic pain in the area of the embolus) with 24 patients with pulmonary embolism but without infarction. Only 18 of the 41 patients with pulmonary infarction had associated heart disease. Pulmonary infarction was uncommon when emboli obstructed central arteries but frequent when distal arteries were occluded. Follow-up x-ray examination showed that the infiltrates resolved in the patients with pulmonary infarction without heart disease, but persisted when heart disease was present. We suggest that obstruction of distal arteries results in pulmonary hemorrhage owing to an influx of bronchial arterial blood at systemic pressure. Hemorrhage causes symptoms and x-ray changes usually attributed to pulmonary infarction. However, hemorrhage resolves without infarction in patients without, but progresses to infarction in those with, heart disease.

Angiography↗
PubMed1977

Hyperpyrexia complicating low fixed cardiac output.

A 41-year-old woman with end-stage mitral and aortic stenosis developed the cycle of low cardiac output, peripheral vasoconstriction, increased core temperature, and cardiac decompensation. This was interrupted by core cooling utilizing iced gastric lavage. We propose that her severe hyperthermia was caused or abetted by her low cardiac output.

Adult↗
PubMed1975

Return of arterial PO2 values to baseline after supplemental oxygen in patients with cardiac disease.

Serial arterial PO-2 values were obtained following discontinuation of supplemental inspiratory oxygen by face mask in 21 patients suffering from a variety of cardiac diseases. All patients were free of pulmonary disease. Arterial PO2 values returned to baseline within seven minutes after supplemental oxygen was withdrawn. Decay rate constants calculated from the arterial PO2 measurements were unaffected by cardiac index or the level of pulmonary capillary wedge pressure. We conclude that in patients free of overt pulmonary disease, arterial PO2 measured five to seven minutes after withdrawal of supplemental inspiratory oxygen accurately reflects an individual patient's baseline arterial PO2 value.

Blood Pressure↗