Abstract
It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 ± 6 to 232 ± 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 ± 410 to 2,170 ± 290 ml/min (P < 0.001), mean arterial pressure decreased from 103 ± 5 to 84 ± 4 mmHg (P < 0.001), left atrial pressure increased from 5.9 ± 0.6 to 10.8 ± 0.9 mmHg (P < 0.001), right atrial pressure increased from 2.4 ± 0.5 to 4.8 ± 0.9 mmHg (P < 0.001), total splanchnic intravascular volume did not change (0 ± 2 ml), splenic intravascular volume decreased 11 ± 3% (P < 0.001), hepatic intravascular volume increased 12 ± 2% (P < 0.001), and mesenteric intravascular volume did not change (-3 ± 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.
Original language | English (US) |
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Pages (from-to) | H1361-H1364 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 262 |
Issue number | 5 31-5 |
DOIs | |
State | Published - 1992 |
Externally published | Yes |
Keywords
- cardiac output
- intravascular capacity
- liver
- mesentery
- pacing tachycardia
- radionuclide imaging
- spleen
- veins
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)