| Hemodynamic Responses and Oxygen Availability in Unanesthetized Dogs during Apnea. |
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Dae Lim Jee, Jun Man Park, Seong Kee Kim, Jae Kyu Cheun |
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| Abstract |
BACKGROUND
This study examined hemodynamic variables, oxygen delivery, extraction, and consumption in response to acute progressive hypoxia and hypercarbia in the setting of apnea.
METHODS
Apnea was induced in 9 healthy mongrel dogs by disconnecting animals from mechanical ventilation of 30 minutes with pure oxygen. Hemodynamic variables, oxygen transport, extraction, and consumption were rapidly and repeatedly measured using pulmonary arterial and arterial catheters until cardiac output was undetectable.
RESULTS
The baseline PaO2, PaCO2, pH, base excess were 318 +/- 137 mm Hg, 36 +/- 3.5 mm Hg, 7.30 +/- 0.06, 6.81 +/- 2.65 mmol/l respectively. Hypercarbia and hypoxemia (76 +/- 33 mm Hg) was first noted at 1 and 4 minute respectively.
Base excess was not changed. Indices of preload (PCWP and CVP) were increased early in the time course (p<0.05). In contrast, indices of afterload (SVR) increased later, just before cardiac decompensation began (p<0.05). No significant reduction of cardiac output, oxygen delivery, extraction, and consumption was detected just until abrupt cardiac decompensation started, 5 minute.
CONCLUSIONS
These data suggest that the early increase in preload was primarily due to hypercarbia whereas the late increase in afterload was due to hypoxemia, but the main cause of acute cardiac decompensation was a critical decrease in arterial oxygen tension with some contribution of increased preload and afterload. |
| Key Words:
Acid-base equilibrium, acidosis; Heart, cardiac output, hemodymics; Oxygen, consumption; Ventilation, apnea |
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