Chest
Volume 100, Issue 2, August 1991, Pages 470-473
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Laboratory and Animal Investigations
Effects of Heart Rate and Pulmonary Artery Pressure on Doppler Pulmonary Artery Acceleration Time in Experimental Acute Pulmonary Hypertension

https://doi.org/10.1378/chest.100.2.470Get rights and content

Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time.

(Chest 1991; 100:470-73)

Section snippets

METHODS

Nine Duroc 50- to 90-kg swine were anesthetized with intramuscular ketamine (25 mg/kg), endotracheally intubated, and maintained anesthetized on a ventilator using 0.5 to 2.0 percent halothane. Surgical cutdowns were performed on the right and left carotid arteries and veins. A 7.5-French (Fr) Could balloon-tipped flow-directed pulmonary artery thermodilution catheter was advanced under fluoroscopic guidance into the right pulmonary artery. An arterial pressure line was established in the right

RESULTS

The mean pulmonary pressure for anesthetized swine in sinus rhythm was 14 ± 4 mm Hg (see Table 1). The mean pulmonary artery pressure was easily varied by either bead injection or pulmonary clamping up to 45 mm Hg. Incremental injections of beads were performed at 30-minute intervals. This interval was chosen as it took about 30 minutes for the collection of data for all heart rates from 50 to 160 beats per minute at each pulmonary artery pressure. Attempts to raise mean pulmonary artery

DISCUSSION

We have developed a model of acute pulmonary hypertension in swine. Bead-induced pulmonary hypertension does not appear to be reversible. Pulmonary clamping produces reproducible elevations in mean pulmonary artery pressure, with the potential benefit of reversibility of the induced obstruction to pulmonary artery blood flow. Pulmonary artery pressure may be returned toward normal if unacceptable systemic hypotension occurs by removing the clamp. An additional characteristic of the pulmonary

ACKNOWLEDGMENT

The authors would like to acknowledge the superb technical assistance of Alice Allfie, the statistical assistance of Nathan Wong, Ph.D., and the laboratory space provided by Orhan Nalcioglu, Ph.D.

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