Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man

Abstract

1. Plasma concentrations of noradrenaline and adrenaline were measured in 11 anaesthetized patients during normocapnia, hypocapnia and hypercapnia. Hypocapnia was produced by deliberate hyperventilation and hypercapnia by adding carbon dioxide to the inspired gas mixture. 2. With a median (range) arterial partial pressure of carbon dioxide of 4.7 (4.2-5.2) kPa, the median (range) plasma concentration of noradrenaline was 0.41 (0.12-0.94) nmol/l and of adrenaline was 0.15 (0.05-0.31) nmol/l. 3. With an arterial partial pressure of carbon dioxide of 2.6 (2.2-3.3) kPa, there was no change in the plasma concentration of noradrenaline [0.37 (0.12-0.86) nmol/l] or that of adrenaline [0.16 (0.05-0.32) nmol/l]. 4. However, with an arterial partial pressure of carbon dioxide of 10.4 (7.6-13.2) kPa, there were significant increases in the plasma concentrations of both noradrenaline [1.13 (0.79-2.05) nmol/l, P < 0.01] and adrenaline [0.67 (0.20-2.92) nmol/l, P < 0.05]. 5. This is the first demonstration in man that respiratory acidosis causes an increase in plasma concentrations of catecholamines.

Effects of an alveolar recruitment maneuver on cardiovascular and respiratory parameters during total intravenous anesthesia in ponies

“…64 Absence of barotrauma was also reported in the clinical setting for human patients by use of airway pressures of 50 to 65 cm H 2 O (V T of 18 mL/kg) during general anesthesia 16 or even 80 cm H 2 0 in patients with ARDS and chest trauma. [62][63][64][65][66][67] Results of 1 study 24 indicate that it is not the high airway pressure but rather the large regional V T that causes lung injury. 24 In our study, a V T of as much as 23 mL/kg was used.…”

“…Hypocapnia (PaCO 2 < 30 mm Hg) should be avoided because it carries the risk of decreased cerebral blood flow 62 and diminished catecholamine release with debilitation of the cardiovascular system. 63 Prevention of excessive hypocapnia during RM is facilitated by continuous monitoring of PaCO 2 and includes a reduction of the respiratory rate; limiting ∆P by increasing PEEP; or, alternatively, the addition of CO 2 to the inspiratory gas.…”

Persistent, progressive hypophosphataemia after voluntary hyperventilation

“…Potential explanations include alterations in acid-base status [4,9] and glucose metabolism [4,9]. Sympathetic activity [20] may also affect serum phosphate, although this is an unlikely cause of HV-induced hypophosphataemia, as respiratory alkalosis has been associated with a decrease in sympathetic activity in a number of studies [21][22][23].…”

Persistent, progressive hypophosphataemia after voluntary hyperventilation

“…In their study, serum phosphate was measured at baseline, during the period of HV and at 75 min after cessation of HV. Sympathetic activity [20] may also affect serum phosphate, although this is an unlikely cause of HV-induced hypophosphataemia, as respiratory alkalosis has been associated with a decrease in sympathetic activity in a number of studies [21][22][23]. When next measured, after 75 min of recovery, serum phosphate remained significantly low, but was returning to normal.…”